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Official websites use. Share sensitive information only on official, secure websites. This article was submitted to Cellular Neuropathology, a section of the journal Frontiers in Cellular Neuroscience. The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner s are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. The gut endocannabinoid system also regulates gut motility, permeability, and inflammatory responses. Furthermore, microbiota composition has been shown to influence the activity of the endocannabinoid system. This review examines the interaction between microbiota, intestinal endocannabinoid system, metabolism, and stress responses. We hypothesize that the crosstalk between microbiota and intestinal endocannabinoid system has a prominent role in stress-induced changes in the gut-brain axis affecting metabolic and mental health. Inter-individual differences are commonly observed in stress responses, but mechanisms underlying resilience and vulnerability to stress are far from understood. Both gut microbiota and the endocannabinoid system have been implicated in stress resilience. We also discuss interventions targeting the microbiota and the endocannabinoid system to mitigate metabolic and stress-related disorders. Keywords: endocannabinoid system, gut microbiota, metabolism and obesity, stress, stress resilience, gut-brain axis. Over the last two decades, a plethora of studies have clearly established the role of the gut microbiota in various metabolic, neurological, and psychiatric disorders. The gut-brain connection is instrumental in molding our physiology, emotional behavior, and stress response Cathomas et al. Stress defines a state of mental and physical tension resulting from adverse or demanding circumstances. Therefore, any change and imbalance in the gut microbiome affect our mental and metabolic health. The endocannabinoid eCB system has been shown in rendering physiological and behavioral resilience to stress and now seems to play a part in the regulation of gut-brain axis. Cannabis has been in use since several thousands of years for medical, religious, and recreational purposes. The role of the eCB system is largely homeostatic in nature and provides resilience to the body to cope with internal and external adverse conditions. In the central nervous system, the eCB system plays crucial roles in the regulation of stress responses, and allostatic alterations in eCB system activity can lead to behavioral and metabolic disorders Cani, ; Iannotti and Di Marzo, Although cannabinoids have therapeutic potential in various neurological disorders, however, the use of synthetic and phytocannabinoids targeting the eCB system faces many challenges, owing to multiple receptors and ligands acting through different mechanisms Di Marzo, In this review, we summarize the role of the eCB system in gut physiology, stress response and its crosstalk with the gut microbiome. The preparations from the cannabis plant Cannabis sativa e. They have been used to treat various ailments, including pain, insomnia, anxiety, lack of appetite, and gastrointestinal GI discomfort. The eCB system was identified about 30 years ago while investigating the mechanism of action of THC, the psychoactive component of cannabis. The eCB system participates in a plethora of physiological functions, including stress coping, anxiety, fear responses, social behavior, and energy storage Silvestri and Di Marzo, ; Lutz et al. Notably, the eCB system has been found to be altered in several pathological conditions such as anxiety disorders, post-traumatic stress disorder PTSD , depression, autism, eating disorders, and irritable bowel syndrome IBS along with others. To understand the variety of its functions, the eCB system has been viewed as a homeostatic system instrumental, e. Despite the crucial role of the eCB system in controlling multiple physiological and pathological processes, only a few compounds acting on this system have been successfully developed for therapeutic purposes Maldonado et al. A better understanding of the roles of eCB system in health and disease will help to lead to therapeutic strategies minimizing the risk associated with the use of cannabinoid receptor agonists. While CB2R is highly expressed in the immune system Munro et al. Presynaptic CB1R is involved in the canonical eCB-mediated suppression of excitatory or inhibitory synaptic transmission. Besides presynaptic location in neurons, CB1R is also present at post-synaptic terminals Maroso et al. CB1R is also present in peripheral tissues although at much lower levels, including adipose tissues, liver, skeletal muscles, kidney, pancreas and GI tract Cavuoto et al. A widespread expression in various peripheral organs has also been reported for CB2R Rogers, ; Bie et al. Endocannabinoids are lipids derived from the membrane phospholipids, and different and redundant pathways have been identified for their synthesis and degradation Muccioli, Notably, these pathways also lead to the production of other bioactive lipids, for example, anti-inflammatory palmitoyl ethanolamide PEA Esposito et al. It is noteworthy to consider these other bioactive lipids in pharmacological approaches targeting the pathways involved in synthesis and degradation of endogenous ligands. The cannabis plant contains more than 80 phytocannabinoids. Therefore, phytocannabinoids have a more enriched pharmacological profile than modulating only cannabinoid receptors, and the number of molecular targets is steadily increasing. Notably, the phytocannabinoid CBD has drawn considerable attention as a treatment option for anxiety, PTSD, depression, autism, or schizophrenia Fiani et al. CBD application in chronic pain and inflammation Argueta et al. CB1R is localized in different components of the gut, such as epithelium, smooth muscle, submucosal myenteric plexus, and the myenteric ganglia Wright et al. In contrast, CB2R is mainly localized in the plasma cells and macrophages in the GI mucosa and submucosa Wright et al. The small intestine and colon show high activity of FAAH, especially during gut inflammation Izzo et al. The endocannabinoid system in the gastrointestinal tract. The crosstalk between the intestinal eCB system and microbiota regulates many GI functions, such as gut permeability, motility, hormonal secretion, nutrient absorption and immune response. CB1R is expressed in different cells in the gut, including epithelial cells colored in violet and different types of enteroendocrine cells colored in yellow, L cell; blue, K cell, and green, I cell, respectively in the mucosa layer. In the myenteric and submucosa plexus, CB1R is present in the enteric nervous system, in particular, in the cell bodies of cholinergic neurons containing the neurotransmitter acetylcholine ACh. Furthermore, CB1R is expressed in the afferent vagal neurons. CB2R is expressed in immune cells as well as in the epithelial cells in the mucosa. MAGL is expressed in the mucosal and muscular layer of the ileum, duodenum, and colon. The highest activity of MAGL is reported in the duodenum, while lowest activity is observed in the distal part of the colon. MAGL is also expressed by the myenteric neurons, where colocalization mainly with the calretinin-positive neurons is reported, while no colocalization could be observed with the nitric oxide synthase NOS expressing neurons Duncan et al. It is prominently expressed by the myenteric plexus and is co-localized with ChAT. In the model of IBS, TRPV1 was found to be dysregulated, and the treatment with eCBs or phytocannabinoids restored its normal physiological function, highlighting the importance of this receptor in gut physiology and pathophysiology De Petrocellis et al. However, their expressions in the GI tract have not been investigated thoroughly and contrary results exist Morales et al. Endocannabinoids are synthesized in different parts of the gut, and their levels change depending upon the metabolic and inflammatory status. In a sham feeding rat model, the levels of 2-AG and AEA increase after orosensory exposure of dietary fats in a vagus nerve-dependent manner. Interestingly, this effect was absent with the carbohydrate or protein intake DiPatrizio et al. In obese human subjects compared to lean and overweight control, elevated levels of fasting plasma AEA are observed while duodenal expression of gap junction proteins, intestinal alkaline phosphatase IAP and zonula occludens ZO-1 , decrease and correlate negatively with the plasma AEA levels Little et al. In rodents, increased obesity is associated with the increased levels of 2-AG and AEA in the duodenum both during fasting and refeeding Izzo et al. Thus, the metabolic status can affect the gut eCB levels and gut permeability. Contrarily, in intestinal inflammation induced by croton oil, no differences in the levels of 2-AG and AEA are observed in the small intestine of control and treated mice. However, the upregulation of CB1R expression is observed in croton-oil induced inflammation. Interestingly, inflamed small intestine showed two-fold higher activity of the AEA degrading enzyme anandamide amidohydrolase Izzo et al. Similarly, in humans, AEA and 2-AG tonically inhibit cholinergic contractility of colonic longitudinal and circular muscles independent of cannabinoid receptor-mediated pathways Smid et al. Furthermore, the genetic ablation of MAGL increases 2-AG levels, however, does not affect the gut transit time, possibly owing to desensitization of CB1R as evidenced by the increased immunohistochemical localization of CB1R in endocytic vesicles Taschler et al. However, there are several other neurotransmitters known to affect gut motility, which can be modulated by the gut eCB system. AEA decreases while CB1R blockade increases both, the ascending contraction, and the descending relaxation, by modulating the levels of substance P and vasoactive intestinal peptide VIP Grider et al. Thus, eCBs can inhibit the gut motility both by inhibiting the excitatory cholinergic neurons and inhibitory VIP motor neurons as well as by inhibiting the CGRP neuron-mediated initiation of peristaltic reflex Grider et al. Gut permeability and nutrients absorption are modulated during various physiological and pathophysiological conditions. The pathological conditions, such as obesity, diabetes, and the inflammation of the gut, affect gut permeability and nutrient absorption. The dysregulation of the eCB system in gut is observed in various pathophysiological and inflammatory conditions. Inflammatory bowel diseases IBD is associated with the impaired epithelial barrier function and increased gut eCB system activity Gassler et al. Interestingly, eCBs and phytocannabinoids have been shown to exert opposite effects on gut permeability. In the cell culture model, AEA and 2-AG increase the permeability of human colorectal adenocarcinoma Caco-2 cell monolayer and synergize with the cytokines to enhance the permeability in a concentration dependent manner Alhamoruni et al. More recently, Caco-2 cell permeability induced by hypoxia can be modulated by eCBs, thus presenting a novel therapeutic target against gut disorders caused by the increased permeability Karwad et al. In addition, enterochromaffin cells secrete neurotransmitters including serotonin, which regulate gut motility and act on afferent and efferent nerves of the enteric nervous system to modulate the gut-brain axis Matthes and Bader, Indeed, eCB signaling in the small intestine has been implicated in the suppression of meal-induced CCK release in obesity Argueta et al. K-cells synthesize and secrete gastric inhibitory peptide GIP , while L-cells secrete glucacon-like peptide 1 GLP-1 in response to nutrient ingestion. Recently, in obese humans, nabilone, a synthetic cannabinoid, increases both fasting and post-glucose intake GIP levels while reduces post-glucose intake GLP-1 levels Chia et al. Furthermore, in vitro studies performed on murine K-cells confirm the inhibitory effect of methanandamide on GIP release Moss et al. In addition to classical cannabinoid receptors, GPR transcripts have been detected in L-cells. GPR55 has been shown to affect energy homeostasis, adipogenesis and insulin secretion Lipina et al. Interestingly, GPR55 is expressed in gut epithelium and the enteric nervous system, suggesting its neuroendocrine role in controlling gut physiology Schicho et al. In addition, CB1R is located on vagal afferent neurons and enterochromaffin cells, suggesting its role in gut neurotransmitter release and gut-brain axis Burdyga et al. The roles of microbiota in gut physiology and gut brain-axis have been convincingly established. The role of microbiota in modulating intestinal eCB tone was first revealed by Rousseaux et al. The role of gut microbiota in intestinal eCB tone regulation was further confirmed by manipulating the gut microbiota by various means, such as antibiotic treatment, probiotic treatment, high fat diet HFD , and by mutations in the Myd88 gene which disrupt TLR-mediated bacteria-host interaction Everard et al. Contrarily, another study showed the up-regulation of colonic CB2R in dysbiotic mice, but the down-regulation of colonic CB1R Aguilera et al. Recently, Akkermansia muciniphila has been identified as an important bacterium regulating the gut eCB tone, gut permeability and secretion of gut peptides Everard et al. Furthermore, the oral treatment with CB1R antagonist SRA increases Akkermansia muciniphila , and decreases Lachnospiraceae and Erysipelotrichaceae in obese mice compared to control group Mehrpouya-Bahrami et al. Similarly, dysbiosis induced by a cocktail of antibiotics decreases AEA level in the duodenum, while probiotic treatment significantly increases AEA level in the jejunum Guida et al. Thus, the microbiota can regulate the intestinal eCB tone. Conversely, the changes in intestinal eCB tone might affect the microbiota composition. These alterations in the gut microbiota were mainly due to changes in 2-AG level which were further confirmed, in vitro , by the culture of fecal microbiota in the presence of 2-AG Dione et al. The increased eCB levels can also modulate the host susceptibility to infections. A recent study suggests that mice with increased 2-AG levels are protected from Enterobacteriaceae pathogens Ellermann et al. The murine attaching and effacing pathogens such as Citrobacter rodentium or Salmonella typhimurium are less virulent in mice with increased 2-AG levels, owing to the antagonizing effect of 2-AG on the bacterial receptor QseC and the subsequent activation of type III secretion systems T3SS. This study further confirms that the genetic ablation of MAGL renders mice less susceptible to intestinal diseases caused by Citrobacter rodentium Ellermann et al. Therefore, a close and bidirectional relationship between gut microbiota and gut eCB tone exists, and thereby can modulate each other. Further studies from germ-free GF mice confirm the effect of microbiota on intestinal eCB tone. The expression of CB1R in the ileum of GF adult mice increases by twofold, which can be partially reversed by the transfer of feces from conventionally raised mice Manca et al. The eCBs levels also showed significant changes in the small intestine of GF mice. The role of gut eCBs in diabetes has also been envisaged given the role of eCBs in regulating the intestinal permeability. In fact, eCBs can regulate the circulating bacterial lipopolysaccharide LPS levels by modulating the gut permeability, which is associated with a low-grade inflammation, insulin resistance and obesity de La Serre et al. Conversely, metabolic endotoxemia induced by the LPS infusion causes obesity and insulin resistance Cani et al. Consequently, the antibiotic treatment reduces gut inflammation and the cecal content of LPS, which is also associated with a sharp reduction in the colonic CB1R levels Cani et al. In addition, the gut eCB system can control dietary fat intake and food preference. Furthermore, fat feeding, particularly the dietary unsaturated fats, increases 2-AG and AEA levels in the jejunum. Consequently, the local infusion of the CB1R antagonist rimonabant into the duodenum inhibits fat intake, an effect mediated through the vagus nerve and the gut-brain axis DiPatrizio et al. High fat and palatable diet alter the intestinal eCB system and microbiome composition Lacroix et al. The palatable diet increases 2-AG and AEA levels in plasma and affects the relative abundance of several intestinal microbiota. Furthermore, a weight-independent correlation exists between the relative abundance of microbiota and the AEA levels Lacroix et al. Everard et al. Furthermore, switching from Western diet to isocaloric Mediterranean diet decreases plasma 2-AG levels, increases plasma OEA and PEA levels, and increases fecal Akkermansia muciniphila abundance, independent of the changes in body weight Tagliamonte et al. However, it is not clear whether the inflammation is caused by the changes in gut metabolites and gut microbiota, or the changes in gut microbiome is a consequence of IBD. Furthermore, several studies have confirmed the therapeutic potential of modulators of eCB biosynthesis and degradation in IBD Alhamoruni et al. The pharmacological inhibition of FAAH has been shown to reduce inflammation and to promote gut healing Sasson et al. Cannabinoid receptors also mediate the low-carbohydrate diet-induced improvement in the gastro-intestinal function and provide protection to the intestinal crypt base Gigante et al. In the mouse model of chemical-induced colitis, CB1R protects from the pro-inflammatory responses, while the genetic deficiency of CB1R induces stronger inflammatory responses Massa et al. In contrast, chemical-induced colitis increases the percentage of CB1R-expressing myenteric neurons, while the cannabinoid receptor agonist HU or the genetic ablation of FAAH protects from the chemical-induced colitis Massa et al. Similarly, mustard oil-induced transient colitis and inflammation is found to be associated with the accelerated transit of upper GI tract, which is accompanied by an increase in the levels of intestinal AEA and decrease in the TRPV1 mRNA levels Capasso et al. This finding was further confirmed in the Chinese population, showing the susceptibility to IBS in patients with the longer alleles of AAT triplet repeat Jiang et al. Contrarily, this association could not be established in the Caucasian population Camilleri et al. Therefore, apparently, there might be ethnic differences in the genetic polymorphism in eCB system related genes. Gastrointestinal cancer is often associated with the chronic gut inflammation, which is an important risk factor in cancer initiation and tumor invasion. Several studies have elucidated the link between dysregulated eCB system, chronic gut inflammation and cancer Hermanson and Marnett, ; Lee et al. Therefore, the microbiota mediated dysregulation of eCBs and concomitant chronic gut inflammation can be a causative link for GI cancer. Due to increased consumption of Western diets, a rapid increase in esophageal adenocarcinoma has been observed mainly owing to obesity and gastroesophageal reflux disorder. Certain microbiota such as Actinobacillus , Campylobacter , Prevotella , Streptococcus , Veillonella , and Leptotrichia are found enriched in the Barrett esophagus, a pre-cancerous lesion. In esophageal squamous cell carcinoma, the most abundant species are Porphyromonas gingivalis , and Veillonella parvula while Peptococcus, Moryella, Corynebacterium, Catonella, Lautropia , Bulleidia, Moryella , Peptococcus , Cardiobacterium , and Treponema genus is depleted Chen X. In human patients with esophageal carcinoma, CB1R gene mutation has been shown to affect tumor susceptibility Bedoya et al. The main gut microbiota which has been implicated in the gastric cancer is Helicobacter pylori and it is suspected to facilitate and prime the gastric mucosa for carcinogenesis, as it is not found in the adrenocarcinoma stage Ferreira et al. The inhospitable pH of the stomach makes difficult for other bacteria to inhabit. However, with the use of advanced techniques, microbiota such as Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria, and Fusobacteria have been detected in the stomach Eun et al. Contrary to gastric cancer, numerous microbial species have been involved in colorectal cancer. In the colon, some gut microbiota have protective roles against cancer, while others are pro-oncogenic. The microbiota producing SCFAs, such as acetate, butyrate, and propionate, have a protective role against cancer. Butyrate has been shown to have a strong preventive and therapeutic effects on cancer in mouse and cellular models Donohoe et al. The eCB system has been implicated in colorectal cancer, and elevated levels of eCBs are found in adenomas as compared to healthy control Zaiachuk et al. A recent study suggests that during inflammation or carcinogenesis, the expression of CB1R decreases in enterocytes due to epigenetic changes in CB1R promoter region Zhang et al. The methylation in the CB1R gene has been positively correlated with the progression of colorectal cancer affecting the tumor size, depth of invasion, and tumor stage. Contrary to this, the activation of GPR55, has been shown to promote tumor growth in various types of cancer and alters the populations of myeloid-derived suppressor cells and T lymphocytes within the tumor tissues Hasenoehrl et al. In a recent study, colorectal cancer patients with metastasis have shown a low expression of CB1R Tutino et al. Interestingly, CB1R downstream signaling pathways were also altered in the normal mucosa surrounding the tumor, suggesting a molecular mechanism underlying malignant transformation. As discussed in detail in the previous section, the gut microbiota interacts with the intestinal eCB system to regulate gut permeability and inflammation. Therefore, dysbiosis and dysregulation of the intestinal eCB system can promote the pathological conditions which increase the susceptibility to colon cancer. Several studies have suggested the therapeutic potential of synthetic and plant-derived cannabinoids, however, the lack of sufficient preclinical data, often compounded with the multiple receptors mediating their effects, are major obstacles for their clinical use Di Marzo and Piscitelli, ; Hryhorowicz et al. Multiple studies have confirmed the role of both exogenous cannabinoids and eCB signaling in providing protection against the gut inflammation in IBD Naftali et al. Only limited preclinical studies in humans using cannabis for the treatment of IBD are available due to legality issues associated with its use. However, a few studies available on humans do not suggest any drastic improvement in the inflammatory markers, however, most of the patients using cannabis report improvement in the discomfort and pain associated with IBD Picardo et al. CBD has been shown to have therapeutic potential in neurodegenerative disorders Cassano et al. PEA is an endogenously produced eCB-like compound, which has been shown to have therapeutic potential in neurodegenerative disorders, inflammatory diseases, and pain perception Petrosino and Di Marzo, Cannabis extracts and THC, when administered orally, have been shown to affect gut motility by modulating the cholinergic transmission Chesher et al. Later, several other synthetic cannabinoids were shown to modulate emesis, suggesting its possible therapeutic use Sharkey et al. Despite the therapeutic potential of exogenous cannabinoids in several gastro-intestinal diseases in rodent models, their therapeutic use has not yet been approved in humans. However, more clinical studies for the use of cannabinoids in humans are required. Multiple studies have convincingly established that the changes in gut microbiota induced by antibiotic, probiotic and GF conditions can lead to behavioral dysregulation related with emotion, anxiety, and stress coping. Conversely, stress and neuropsychiatric disorders can perturb the microbiota composition. Therefore, this strongly suggests the existence of a bidirectional communication between gut and brain, called the microbiota-gut-brain axis Figure 2. Many studies suggest the role of gut neurotransmitters and hormones in the modulation of host-bacteria interaction and virulence. Furthermore, the presence of interaction sites for these hormones on bacteria has been shown Hughes and Sperandio, HKs have both kinase and phosphatase activity, and cellular signals can either activate or deactivate. Recently, the highly abundant neurotransmitter serotonin, which is also secreted from enterochromaffin cells in the gut lumen, was shown to decrease the virulence of enterohemorrhagic Escherichia coli and Citrobacter rodentium in rodents. The binding site for serotonin is a membrane-bound histidine sensor kinase, CpxA, which inactivates the transcription factor CpxR after dephosphorylation induced by serotonin, controlling the virulence gene. Interestingly, CpXA is also expressed by other gut bacteria. Thus, serotonin can affect the microbiota composition and virulence Kumar et al. Microbiota-gut-brain axis in the regulation of stress responses and metabolism. Mechanisms underlying the bidirectional communication include the vagus nerve, immune system, circulating mediators and HPA axis. Microbiota composition is affected by stress, diet, prebiotics, postbiotics and antibiotics among other factors. Conversely, microbiota composition can affect the release of gut hormones and neurotransmitters and can communicate with the brain via the vagus nerve Figure 2. Studies using GF mice suggest deficient circulating and colon serotonin levels as compared to specific-pathogen free SPF mice Wikoff et al. The gut microbiota can regulate serotonin synthesis both in mice and humans. In GF mice, the colonization of spore-forming bacteria increases serum serotonin and the colonic expression of tryptophane hydroxylase 1 TPH1 Yano et al. Interestingly, the colonization of GF mice with spore-forming bacteria from human colonic microbiota yields the same effects on serotonin levels, thus suggesting that the effects of these microbes on serotonin synthesis is conserved across mice and humans Yano et al. Enteroendocrine cells respond to gut metabolites and modulate the secretion of GI hormones, thereby regulating food intake, satiety, and gut motility Wu et al. Gut hormones and neuropeptides, such as CCK, PYY and GLP-1 through its binding sites on the vagus nerve, communicate with the brain to regulate behavioral and metabolic processes. The vagus nerve mediates the bidirectional communication between the brain and the gut microbiota Bellono et al. Recently, it has been shown that LPS-induced depression-like phenotype and alterations in the gut microbiota diversity are not observed after subdiaphragmatic vagotomy, indicating the vagus nerve-mediated communication between the gut and the brain Zhang et al. Several earlier studies also confirmed that oral administration of intestinal bacteria, such as Campylobacter jejuni and Lactobacillus rhamnosus , induces c-fos activation in brainstem regions receiving afferent sensory information from the GI tract and produce region-specific changes in GABAB1b receptor expression in the mouse brain Gaykema et al. Furthermore, these changes can lead to stress-induced corticosterone CORT release, and anxiety and depression-like behavior. These effects are mediated by the vagus nerve, as resection of the vagus nerve abolishes these effects, suggesting a constitutive communication between brain and gut via the vagus nerve Bercik et al. Interestingly, this effect was absent when antimicrobials were administered intraperitoneally, suggesting the intermediary role of neurally active metabolites secreted from the gut microbiota Bercik et al. Microbial metabolites, such as indole, produced by the gut microbiota through the enzyme tryptophanase have been shown to modulate the gut-brain axis Kumar and Sperandio, ; Figure 2. GF rats, when transplanted with bacterial species overproducing indole, exhibit increased anxiety-like behavior, which is primarily due to the increased vagus nerve activation Jaglin et al. In mice, chronic indole production does not cause behavioral changes, but it does affect behavior under duress and increases the susceptibility of male mice to chronic mild stress Mir et al. Furthermore, this study showed that indole increases the expression of the phenylethanolamine N -methyltransferase PNMT gene in the adrenal medulla and thus affects the synthesis of noradrenaline. The SCFAs, such as the acetate, propionate, and butyrate, are also produced by microbiota in the colon, which have been implicated in the behavior and several neurophysiological disorders Silva et al. The vagus nerve acts as a bidirectional communication pathway between the periphery and the brain and is one of the principal components in the microbiota-gut-brain axis Mayer, ; Prescott and Liberles, ; Figure 2. Importantly, the GI tract is highly innervated by both efferents and afferents of the vagus nerve. The efferent vagal preganglionic fibers from the dorsal motor nucleus vagus DMV innervate postganglionic neurons located in the myenteric and submucosal plexus of the gut Berthoud and Neuhuber, Furthermore, the vagus afferents include the primary sensory neurons that convey both mechanical and chemical information from the GI tract to the brain Han et al. The cell bodies of these sensory neurons are located in the nodose ganglia, which send bipolar axons to both the GI tract and the nucleus tractus solitarius NTS. From the NTS, the vagal nerve can regulate via few synapses the neuronal activity of e. Han et al. They mapped the neuronal circuit that connects the right vagal nodose ganglia to nigral dopamine neurons using an anterograde transynaptic viral tracer. The mapping approach elucidated a reward circuit consisting of the right nodose ganglia, the parabrachio-nigral pathway and its target in the dorsal striatum Han et al. Similarly, as postulated previously Craig, , the vagal afferents might influence the regulation of emotional responses by sending interoceptive inputs via NTS-parabrachial nucleus-thalamus pathway to insula cortex Mayer, The insula cortex also referred as interoceptive cortex is an integrative hub that is highly connected to amygdala, ventral striatum and prefrontal cortex Gehrlach et al. Notably, it has been reported that CB1R is expressed in vagal afferents innervating different regions of the GI tract Vianna et al. Overall, the vagal nerve is a critical component of the microbiota-gut-brain axis in the regulation of food intake, hedonic feeding, visceral pain, aversion and emotions, but the anatomical mapping of the underlying circuits is still poorly understood. Dietary components and specific amino acids, such as glutamine and tryptophan, affect the crosstalk between microbiome and gut permeability Chakaroun et al. The gut permeability can be modulated by microbial metabolites such as SCFAs produced from the metabolism of dietary fibers Chen et al. In rodents, HFD alters gut microbiota, and bile acid metabolism, leading to increased levels of inflammatory cytokines and increased gut permeability Stenman et al. Furthermore, prolonged dietary intake of HFD decreases tight junction proteins expression claudin-1, claudin-3, occluding and junctional adhesion molecule-1 in small intestine Suzuki and Hara, The gut microbiota control the intestinal eCB tone and therefore, affect gut motility and gut permeability. CB1R blockade improves gut barrier function and alters the levels and distribution of ZO-1 and occluding gap junction proteins, while increasing eCB tone enhances the gut permeability and increase plasma LPS levels Muccioli et al. The allogenic transplantation of fecal microbiota from lean donor to male recipient with metabolic dysregulation improves insulin sensitivity and affects plasma level of GABA Kootte et al. Importantly, serotonin secretion from enterochromaffin cells is microbiota-dependent and therefore, gut motility can be modulated by gut microbiota by altering the levels of neurotransmitter release from the enteric nervous system Yano et al. The analysis of enteroendocrine cell number and distribution in SPF and GF mice suggests the upregulation of enteroendocrine cell numbers, specifically the enterochromaffin cells, K-cells and L-cells Modasia et al. The microbiota composition in human subjects with metabolic disorders, such as type 2 diabetes, obesity and associated metabolic complications including hyperlipidemia, atherosclerosis, and hepatic steatosis, differs from that of healthy humans, suggesting its role in whole-body metabolism Turnbaugh et al. GF mice have less total body fat and body weight gain compared to SPF mice despite having higher food intake, thus confirming the role of microbiota in metabolic regulation Turnbaugh et al. The effect of microbiota on host metabolism is mediated by the gut-brain axis and microbial metabolites, affecting gut permeability, inflammation, and insulin resistance. Consequently, dysbiosis induced by antibiotics reduces the metabolic endotoxemia and LPS levels in obese mice, leading to improved metabolic profile Cani et al. The gut eCB system has been implicated in gut inflammation and metabolic regulation. CB1R antagonists affect gut microbiota composition, reduce inflammation and M1 macrophages in adipose tissue and plasma LPS level, and therefore reduce intestinal permeability and metabolic endotoxemia Mehrpouya-Bahrami et al. Furthermore, CB1R blockade increases the abundance of Akkermansia muciniphila in the gut, while decreases Lachnospiraceae and Erysipelotrichaceae , confirming the eCB system-mediated changes in microbiota composition Mehrpouya-Bahrami et al. In addition, engineered NAPE-expressing Escherichia coli bacteria, when administered through drinking water, reduces the adiposity in HFD fed mice by reducing food intake, improving insulin sensitivity and reducing hepatosteatosis Chen et al. Thus, manipulating gut eCB signaling by using engineered gut bacteria might have therapeutic potential. In humans, gut microbiota transfer from lean to obese individuals improves the peripheral insulin sensitivity, owing to increased gut microbial diversity Vrieze et al. Prediabetic and overweight Danish adults with insulin resistance and dyslipidemia showed perturbed gut microbiota with low abundance of Akkermansia muciniphila and the genus Clostridium Allin et al. A metagenomic-wide association study suggested the association between type 2 diabetes and gut dysbiosis, a reduction in the butyrate-producing gut bacteria and an increase in the opportunistic pathogenic bacteria Qin et al. Thus, a strong interaction between host genetics, gut microbiota and diet exists, thereby determining the metabolic phenotype. Furthermore, the metabolic phenotype can be manipulated by changing the microbiota composition as suggested by the fecal transplant experiments, establishing the causative role of microbiota in regulating the whole-body metabolism Ussar et al. The mechanism by which microbiota can affect the whole-body metabolism and the inflammation involves the microbial metabolites that reach the circulation and the vagus nerve, thereby affecting the host metabolism, inflammation, and neuroendocrine secretions Cani, ; Scheithauer et al. The elevated level of microbially produced imidazole propionate was found in the portal and circulating plasma of subjects with type 2 diabetes compared to healthy control group Koh et al. Furthermore, this study showed that imidazole propionate impairs insulin signaling through mTORC1 by inhibiting tyrosine phosphorylation of insulin receptor substrates, leading to its proteasomal degradation. Similarly, indole, another bacterial metabolite, reduces the LPS-induced upregulation of pro-inflammatory mediators in liver, and its oral administration before LPS injection reduces the expression of key inflammatory proteins Beaumont et al. The gut microbiota composition has an important impact on the metabolism of ingested food and nutrients. Some metabolites may be linked with the disease pathogenesis such as cardiovascular and metabolic diseases Brown and Hazen, ; Scheithauer et al. The gut microbiota-derived metabolite trimethylamine N -oxide TMAO has been regarded as a risk factor for cardiovascular disease pathogenesis by promoting atherosclerotic lesions. The studies from GF mice indicate the role of dietary choline and TMAO produced from the gut microbiota in atherosclerosis and macrophage cholesterol accumulation Wang et al. Furthermore, the susceptibility to atherosclerosis can be transmitted to otherwise healthy mice by transplanting TMAO-producing gut microbiota obtained by mice fed with a diet rich in choline Gregory et al. Increasing evidence suggests a crosstalk between the eCB system and microbiota in atherosclerosis Moludi et al. The bile acid composition can also affect the composition of microbiota or conversely, microbiota can affect the metabolism of bile acids. The altered metabolism of bile acids has been associated with IBD, metabolic disorders, and colorectal cancer Nagengast et al. The SCFAs, produced by the microbiota Bifidobacterium and Akkermansia muciniphila through intestinal fermentation of dietary fibers, have been inversely related with the low-grade inflammation, insulin resistance and type 2 diabetes Canfora et al. SCFAs, such as butyrate and propionate, can reduce hepatic lipid accumulation, and increase glucose tolerance in the animal models of diet-induced obesity and type 2 diabetes den Besten et al. Numerous studies have confirmed the interaction between gut microbiota and hypothalamic-pituitary-adrenal HPA axis, suggesting that the gut microbiota composition might affect the stress-induced activation of the HPA axis Figure 2. GF rats show increased levels of corticosterone CORT in the open field test compared to SPF rats and show increased expression of stress-related corticotropin releasing hormone CRH in the hypothalamus, while show reduced glucocorticoid receptor GR expression in the hippocampus Crumeyrolle-Arias et al. Postnatal disruption of microbiota colonization can affect the neuroendocrine response and the connectivity of neuronal circuits regulating the stress response. The most striking finding of this study was that the hyperresponsiveness of HPA axis can be corrected by administering Bifidobacterium infantis or transplanting microbiota from SPF mice only during the early stage but not at the later stage, suggesting the role of microbiota in the early programming of neuroendocrine response of the HPA axis Sudo et al. This study further confirmed that the absence of microbiota increases the expression of tyrosine hydroxylase TH , PNMT, melanocortin receptor 2 MC2R , steroidogenic acute regulatory protein StAR and cytochrome P family 11 subfamily A member 1 CYP11a1 in the adrenal, while in the pituitary, it increases the expression of FKB prolyl isomerase 5 gene, which regulates GR sensitivity. In addition to neuronal effects mediated by the gut-brain axis, the metabolites released from the gut microbiota can directly modulate host physiology. Indole produced from the gut bacteria has recently been shown to affect the adrenal medulla in mice and modulate the expression of PNMT gene involved in the catecholamine biosynthetic pathway Mir et al. In rats, chronic prenatal stress leads to the hyperresponsiveness of the HPA axis to stress later in life and affects the development of the enteric nervous system with marked reduction in the colonic innervation density and augmented secretory response of colon after catecholaminergic stimulation Golubeva et al. Furthermore, prenatal stress also alters the microbiota composition and reduces Lactobacillus , while increasing Oscillibacter , Anaerotruncus , and Peptococcus. The HPA response, as measured by the plasma CORT levels in adult offspring 15 min after restraint stress, showed higher activity in vaginally delivered prenatally stressed males compared with the control male offspring. Similarly, stress during pregnancy also affects the microbiota composition of the mother, and the microbiota of both mother and offspring can affect the development and programming of the HPA axis, leading to aberrant HPA response and social behavior later in life de Weerth, ; Gur et al. Early life stress regulates the responsiveness of the HPA axis later in life, and therefore in utero exposure or neonatal stress can lead to dysbiosis and affect the development of the HPA axis. In human infants, it was shown that maternal prenatal stress, as confirmed by the elevated levels of maternal salivary cortisol, perturbs the microbiota composition with significantly increased abundance of Proteobacterial groups and decreased abundance of Lactobacillus and Bifidobacterium , leading to enhanced GI inflammation Zijlmans et al. Similarly, stressed rats pups with limited nesting show increased basal CORT at weaning with decreased microbial diversity and increased gut permeability. This effect was more prominent in females than males, suggesting the influence of sex on microbiota induced changes in the HPA axis Moussaoui et al. In addition to chronic stressors, acute stressors can also affect the colonic microbiota composition. In such experiment, an acute brief exposure to social stressor significantly alters the relative abundance of microbiota, decreasing the beneficial Lactobacillus genus Galley et al. Here, we will summarize those findings that relate the microbiota-gut-brain axis to stress-related disorders Figure 2. In this regard, the first evidence comes from the fact that IBS shows high co-morbidity with stress-related disorders, such as anxiety and depression Whitehead et al. Indeed, it has been proposed that modulation of the microbiota e. Furthermore, the GF mice as animal model are instrumental to elucidate the impact of the microbiota in both health and pathological conditions. In line with these findings, the absence of gut microbiota increases anxiety behavior in GF adult mice Neufeld et al. Importantly, such behavioral phenotype was swapped by gavage administration of the cecal microbiota to GF mice from these two mouse lines, conferring the behavioral profile of the donor Bercik et al. Challenging this notion, some studies found that adult GF mice displayed reduced anxiety-like behavior in comparison to mice with gut microbiota Diaz Heijtz et al. These data put forward the concept that intestinal microbiota influences anxiety-like behavior. Moreover, using animal models of stress, it was described that stress can affect gut microbial composition Gareau et al. Clinical studies also found changes in microbial composition in patients with a diagnosis of depression or anxiety disorder Bastiaanssen et al. These findings suggest that stress induces a dysbiotic state with a decrease in commensal microbiota and an increase in opportunistic pathogens. The underlying mechanisms are complex, bidirectional, and still elusive. Dexamethasone treatment, mimicking the stress response, increased GI permeability Meddings and Swain, Changes in permeability increase mobility of LPS or other endotoxins from the lumen to the host and its interaction with the immune system, promoting the expression of inflammatory mediators in the circulation. In maternal separated rats, probiotic interventions reversed stress-induced behavioral deficits as well as normalized blood cytokines levels Desbonnet et al. Furthermore, pre- and probiotic interventions have been used extensively to investigate the physiological functions of the microbiota-gut-brain axis. While probiotics are living microorganisms that exert beneficial effects on the health of the host after ingestion, prebiotics provide food favoring the growth of beneficial microbes. Several studies described the treatments using prebiotics, postbiotics or the combination of both can mitigate stress-induced anxiety- and depression-like behavior in animal models Gareau et al. For example, chronic treatment for 4 weeks with probiotic Lactobacillus rhamnosus JB-1 caused a decreased anxiety- and depressive-like behavior in healthy mice during elevated plus maze and forced swimming test, respectively, concomitant with a reduced acute stress-induced CORT levels Bravo et al. Lactobacillus rhamnosus modified gene expression levels of the GABAergic system, the main inhibitory neurotransmitter system in the brain, in several key brain areas of the stress system Bravo et al. Notably, the probiotic-related effects on neurochemical changes as well as in behavior were abolished in vagotomized mice Bravo et al. In another study, probiotic treatment diminished the maternal separation stress-induced changes in gut physiology and normalized elevated CORT levels in rats Gareau et al. Additionally, a chronic combined prebiotic treatment protected against chronic social stress-induced anxiety-like behaviors, reduced social interaction, stress-induced elevetations in proinflammatory cytokines, and stress-induced alterations in the microbiome Burokas et al. The beneficial effect of pre- and probiotic interventions on emotional responses seems to be more pronounced following stress. Accordingly, probiotic supplementation was effective in decreasing depressive-like behavior in stressed rats but not in non-stressed rats Desbonnet et al. In healthy humans, probiotic supplementation for 30 days alleviated physiological distress Messaoudi et al. In summary, these findings suggest that specific probiotic strains might be applied as treatment against mental health disorders. It is well established that the eCB system strongly regulates stress response Lutz et al. Regarding the specific role of the intestinal eCB system in the regulation of stress responses, only few studies have addressed this appealing hypothesis. In a fundamental study, Guida and coworkers examined the impact of antibiotic-induced dysbiosis on the intestinal eCB system as well as on depressive-like behaviors Guida et al. In short, antibiotic-induced perturbation of the microbiota caused a depressive-like phenotype in the tail suspension and social interaction test. At the molecular level, the antibiotic-induced dysbiosis led to dramatic changes in the overall gut microbial composition, local inflammation, and decreased AEA levels in the duodenum Guida et al. Importantly, some of these changes were reversed after probiotic administration Guida et al. Concerning the stress-induced changes in gut motility, a peripherally restricted CB1R agonist was able to normalize the stress effects in motility, pointing out that intestinal CB1R is a key regulator of gut dysfunctions caused by stress Keenan et al. In another crucial study, fecal microbiota transplantation of chronic mild stressed mice, a mouse model of depression, caused depressive-like behavior in the recipient mice Chevalier et al. Notably, molecular and behavioral alterations in the recipient mice were linked to a reduced serum lipid precursors for the production of eCB ligands as well as decreased eCB levels in the brain Chevalier et al. Indeed, alterations of the gut microbiota profoundly impact the intestinal eCB tone Manca et al. Alterations of the intestinal eCB system may provide a link between stress and chronic abdominal pain Rousseaux et al. Furthermore, low vitamin D dietary intake-induced allodynia was linked with lowered microbial diversity and reduced 2-AG levels in the colon Guida et al. Interestingly, other studies have pointed out that the CB2R expression in the epithelial cells of the intestine might have an analgesic effect in visceral pain Rousseaux et al. Based on the above evidence, an attractive hypothesis points to the role of the gut microbiota as a potential resilience factor against stress-related pathologies. Indeed, the idea that diet might influence emotional responses has been established many years ago. Some studies found that certain species of bacteria are more abundant in resilient mice in comparison to control or susceptible mice Marin et al. Recently, we have demonstrated differences in gut microbial composition associated with a resilience outcome to a single trauma in mice Pascual Cuadrado et al. Interestingly, we found an increased abundance of A. In another study, oral administration of the probiotic Bifidobacterium increased the number of resilient mice to chronic social defeat paradigm Yang et al. Conflicting results have also been reported and some studies have not found an association between microbiota composition and emotional responses Tsilimigras et al. Both clinical and animal studies described a prominent feature of sexual differences in the incidence of mental health disorders, with almost two-fold higher prevalence of anxiety and depression in women Kessler, ; Goodwill et al. Moreover, alterations in sex-specific microbiota composition may rely on gender sensitivity to environmental factors such as stress reactivity. The mechanistic insights of the sex hormone-related changes in microbial composition are not fully understood yet. In any case, sex differences in the microbiota-gut-brain axis function might contribute to the increased vulnerability of anxiety and depression in both women and female rodents. Nevertheless, it is still an unexplored research area, and more studies are needed to unravel the sexual dimorphism in the microbiota-gut-brain axis related to physiological and pathophysiological functions. Overall, these findings underline the link between microbiota-gut-brain axis and stress responses and point out that underlying mechanisms are complex, intertwined, and bidirectional Figure 2. Indeed, it might also be plausible that several of the described mechanisms are working in parallel. We also put forward the notion that certain gut microbial populations provide resilience to stress-related pathologies, where the intestinal eCB system might play a key role. Furthermore, the aforementioned evidence showed that the crosstalk between microbiota and the intestinal eCB might play a prominent role in the regulation of emotional responses. Further studies will have to elucidate whether it might serve a novel therapeutic target to confer resilience against stressful events. Gut microbiota abundance and composition change during different physiological and pathophysiological conditions such as gut inflammation, obesity, diabetes, and stress Table 1. In chemical-induced colitis models higher relative abundance of orders Enterobacteriales, Verrucomicrobiales, and Deferribacterales while lower abundance of Bacteroidales have been reported Lupp et al. Notably, the relative abundance of the family Bacteroidaceae increases while Rikenellaceae decreases. The relative abundance of Akkermansia increases in dextran sodium sulfate-induced colitis model Berry et al. Similarly, pathogen-induced gut inflammation is associated with increased abundance of Gammaproteobacteria. Mice that are genetically susceptible to gut inflammation, such as IL deficient mice, harbor higher numbers of Escherichia coli than healthy controls Wohlgemuth et al. Metabolic disorders are also associated with the changes in microbiota. In high fat diet fed mice, lower abundance of Bifidobacterial and Eubacterium rectale-Clostridium coccoides group compared to controls have been reported Ley et al. Thus, obesity and metabolic syndrome are closely associated with changes in the diversity of gut microbiota. Similarly, stress exposure can cause gut dysbiosis. In rodents, restraint stress increases relative abundance of gut microbiota belonging to phylum Firmicutes and Deferribacteres while reduces Actinobacteria Galley et al. In addition, social stress caused by exposure of aggressor mice affects the relative abundance of microbiota Gautam et al. Particularly, the phylum Firmicutes and Bacteroidetes are more vulnerable to this kind of stress. The proportion of Firmicutes and Verrucomicrobia decrease after exposure to the aggressor. The social stress in rodents produce the most striking changes in the relative abundance of microbiota in the genus Lactobacillus , Akkermansia , Oscillospira, Coriobacteriaceae , and Anaeroplasma Bharwani et al. In a PTSD mouse model, we recently identified an increased abundance of Akkermansia muciniphila in resilient mice in the analysis of different taxa inhabiting the gut Pascual Cuadrado et al. The prenatal stress and the disruption of mother-infant bond lead to stress related behavioral disorders as well as changes in the gut microbiota. Adult rats exposed to maternal separation show behavioral deficits, which can be reversed by the chronic treatment with Bifidobacteria or by anti-depressive citalopram treatment Desbonnet et al. Furthermore, a significant reduction in Lactobacillus species has also been observed in maternally separated pups Gareau et al. Notably, the decreased numbers of bacteria in the Lactobacillus genus persist in the adulthood at 4 months of age in prenatal stress rats Golubeva et al. In infant rhesus monkeys, the reduction in fecal Lactobacilli is associated with stress-related behavioral deficit Bailey and Coe, Changes in the microbiota composition associated with different pathological conditions in animal models. Hereby, several mechanisms may be involved in, including the regulation of intestinal barrier integrity, influences on immune modulation and on the enteroendocrine system, and mediators from the microbiome passing into the body. The role of the eCB system is particularly apparent in pathological states such as in rodent models of obesity and type-2 diabetes, and gut inflammation e. This is consistent with the fact that the eCB system acts to enable the homeostatic state of the organism and gets into action under internal and external challenges Di Marzo, Chronic treatment of obese rodents with THC led to altered microbiota with an increased Firmicutes:Bacteroidetes ratio, and concomitantly to the reduction of the obese state Cluny et al. Chronic treatment with capsaicin, a TRPV1 agonist, in obese rodents increased the levels of butyrate-producing Ruminococcaceae and Lachnospiraceae , while leading to decreased levels of LPS production. Fecal microbiota transplantation in GF mice showed that capsaicin-induced protection against HFD-induced obesity was transferrable, indicating the crucial role of the microbiota Kang et al. Similarly, in another study, such a treatment was shown to improve glucose homeostasis via GLP-1, and concomitantly, microbiota composition was changed, with increased abundance of Bacteroides genera. Microbiota transplantation experiments revealed that the beneficial effect of capsaicin was transferable Hui et al. CBD has drawn quite some attention due to its various beneficial effects, e. In a recent study, the treatment of mice with CBD-enriched cannabis extracts was investigated on the gut microbiome and associated histomorphological and molecular changes in the mouse gut mucosa Skinner et al. Increases in the relative abundance of the probiotic Akkermansia muciniphila was detected. These observations raise the question on the long-term effects of therapeutic CBD application in humans on the microbiome. Of note, the mice used were not in a pathological state, thus, leaving the issue that the situation might be different if there were an induced pathological state, such as obesity or gut inflammation. Akkermansia muciniphila , a species suggested to mediate anti-inflammatory action in colitis, was increased by the experimental colitis after 12 days, but its levels were significantly elevated by the combined treatment already at day 8, indicating that the treatment intervention enhanced the elevation of Akkermansia muciniphila upon induction of experimental colitis, possibly thereby enabling the beneficial effects of these species. These data reveal the potential of phytocannabinoids in the modulation of the microbiome, and consequently in gut functions, immune status and finally to behavioral changes. Yet, regarding the modulation of stress-related disorders, the evidence is sparse and needs specific investigations, but considering the link between stress and dysregulations of the microbiome and gut functions, such experiments are promising and will shed light onto new aspects of the action of phytocannabinoids. Therefore, further research to unravel the roles of enteroendocrine cells in lipid sensing is required. This is crucial especially when the role of the vagus nerve and gut-brain axis has already been suggested in fat intake. Most of these receptors are also targets of phytocannabinoids. Therefore, further research should shed light on their expression and functional role in the GI tract as well as their interaction with the gut-brain axis. Future studies to investigate the roles of these receptors are warranted to exploit their therapeutic potential in GI and neurological disorder. All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. As a library, NLM provides access to scientific literature. Front Cell Neurosci. Find articles by Raj Kamal Srivastava. Find articles by Beat Lutz. Find articles by Inigo Ruiz de Azua. Received Jan 31; Accepted Mar 14; Collection date Open in a new tab. Animal models Bacterial abundance References Gut inflammation Dextran sodium sulfate DSS -induced colitis model Decrease in phylum Bacteroidetes Increase in order Clostridiales, Verrucomicrobiales, and Anaeroplasmatales Decrease in order Bacteroidales Increase in family Ruminococcaceae, Bacteroidaceae, Enterobacteriaceae, Deferribacteraceae , and Verrucomicrobiaceae Increase in bacteria Enterococcus faecalis Lupp et al. Changes in comparison to the control group. Similar articles. Add to Collections. Create a new collection. Add to an existing collection. Choose a collection Unable to load your collection due to an error Please try again. Add Cancel. Dextran sodium sulfate DSS -induced colitis model. Decrease in phylum Bacteroidetes Increase in order Clostridiales, Verrucomicrobiales, and Anaeroplasmatales Decrease in order Bacteroidales Increase in family Ruminococcaceae, Bacteroidaceae, Enterobacteriaceae, Deferribacteraceae , and Verrucomicrobiaceae Increase in bacteria Enterococcus faecalis. Lupp et al. Citrobacter rodentium CR infection mediated inflammation model. Decrease in phylum Bacteroidetes Increase in phylum Firmicutes, and Proteobacteria Decrease in order Bacteroidales Increase in order Enterobacteriales and Bacillales Increase in family Enterobacteriaceae. Increase in phylum Deferribacteres Increase in bacteria Mucispirillum schaedleri. Vereecke et al. Geurts et al. Ley et al. Decrease in phylum Bacteroides Increase in phylum Firmicutes Increase in class Erysipelotrichi and Bacilli Increase in family Rikenellaceae and Lachnospiraceae Decrease in phylum Bacteroidetes Decrease in genus Prevotella , Lactobacillus and Bifidobacterium Decrease in bateria Eubacterium rectale , and Clostridium coccoides. Cani et al. Bailey and Coe, ; Gareau et al. Golubeva et al. Increase in phylum Firmicutes and Actinomycetota Decrease in family Porphyromonadaceae, and Lactobacillaceae Increase in family Ruminococcaceae and Lachnospiraceae Decrease in genus Tannerella , Lactobacillus, Adlercreutzia, and Sarcina in females Increase in genus Oscillospira , and Bifidobacterium Increased colonization by Citrobacter rodentium, and Ruminococcus gnavus in females but decreased in males. Bailey et al. Decrease in genus Bacteroides Increase in genus Clostridium and Ponticaulis Decrease in family Lactobacillaceae and Porphyromonadaceae Decrease in genus Lactobacillus, Parabacteroides, Akkermansia Decrease in unclassified Firmicutes , and unclassified Bacilli Decrease in genus Bifidobacterium in susceptible mice Decrease in Lactobacillus reuteri. Increase in family Ruminococcaceae and Porphyromonadaceae Decrease in family Lactobacillaceae. Chevalier et al. Increase in genus Bacteroides in resilient mice Decrease in phylum Firmicutes in resilient mice Increase in bacteria Akkermansia muciniphila, Bacteroides acidifacians and Clostridium citroniae in resilient mice. Pascual Cuadrado et al.
The Microbiome and Gut Endocannabinoid System in the Regulation of Stress Responses and Metabolism
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The Microbiome and Gut Endocannabinoid System in the Regulation of Stress Responses and Metabolism
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The Microbiome and Gut Endocannabinoid System in the Regulation of Stress Responses and Metabolism
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