Human-derived gut microbiota modulates colonic secretion in mice by regulating 5-HT<sub>3</sub> receptor expression via acetate production

Bhattarai, Yogesh; Schmidt, Bradley; Linden, David R.; Larson, Eric D.; Grover, Madhusudan; Beyder, Arthur; Farrugia, Gianrico; Kashyap, Purna C.

doi:10.1152/ajpgi.00448.2016

Cited by 73 publications

(59 citation statements)

References 39 publications

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“…In addition to its characteristic as an important neurotransmitter, 5‐HT is also a potent secretagogue and a significant regulatory factor in the digestive tract (Bhattarai et al., ). The majority (90%) of 5‐HT in the body is released from the enterochromaffin (EC) cells and is derived from the hydroxylation of the dietary L‐ Trp (Gershon & Tack, ).…”

Section: Tryptophan Microbiota and The Immune Systemmentioning

confidence: 99%

“…At least seven different families of 5‐HT receptors and fourteen receptor subtypes have been identified (Bhattarai et al., ). Among them, the type 3 serotonin receptor (5‐HT3R) and 5‐HT4R are involved in the host 5‐HT biosynthesis and GI transit modulations via the gut microbiota (Kashyap et al., ); thus, these two receptors are pivotal in regulating intestinal secretion.…”

Section: Tryptophan Microbiota and The Immune Systemmentioning

confidence: 99%

“…This change in GF mice contributes to the increased colonic secretion. In addition, such a secretory response that is dependent upon 5‐HT3R is also observed in humanized (HM) and conventionally raised (CR) mice, suggesting that a relatively conserved microbial function drives this process (Bhattarai et al., ).…”

Section: Tryptophan Microbiota and The Immune Systemmentioning

confidence: 99%

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Dietary Amino Acids and the Gut‐Microbiome‐Immune Axis: Physiological Metabolism and Therapeutic Prospects

2018

Comp Rev Food Sci Food Safe

190

122

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Dietary amino acids (AAs) are not only absorbed and metabolized by enterocytes but also available to the microbiota in the gut in mammals. In addition to serving as the materials for protein synthesis, AAs can act as precursors for numerous metabolic end products in reactions involving the intestinal mucosa and microbiota. After penetrating the epithelial barrier, microbial metabolites can enter and accumulate in the host circulatory system, where they are sensed by immune cells and then elicit a wide range of biological functions via different receptors and mechanisms. Some intestinal bacteria can also synthesize certain AAs, implying that the exchange of AAs between hosts and microorganisms is bidirectional. Changes in AA composition and abundance can affect AA‐metabolizing bacterial communities and modulate macrophages and dendritic cells via toll‐like receptors (TLRs), autoinducer‐2 (AI‐2), and NOD‐like receptors (NLRs), and also regulate the gut‐microbiome‐immune axis via aryl hydrocarbon receptor (AhR), serotonin/5‐hydroxytryptamine (5‐HT), and other signaling pathways, all of which play critical roles in regulating the intestinal mucosal immunity and microbiota directly or indirectly, contributing to intestinal homeostasis. Therefore, the current findings of the effects of certain functional AAs on the gut‐microbiome‐immune axis are reviewed, illustrating signaling pathways of tryptophan (Trp), glutamine (Gln), methionine (Met), and branched‐chain AAs (BCAAs) in the intestinal barrier and regarding immunity via crosstalk with their receptors or ligands. These findings have shed light on the clinical applications of dietary AAs in improving gut microbiota and mucosal immunity, therefore benefiting the gut as well as local and systemic health.

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Section: Tryptophan Microbiota and The Immune Systemmentioning

confidence: 99%

Section: Tryptophan Microbiota and The Immune Systemmentioning

confidence: 99%

Section: Tryptophan Microbiota and The Immune Systemmentioning

confidence: 99%

See 1 more Smart Citation

Dietary Amino Acids and the Gut‐Microbiome‐Immune Axis: Physiological Metabolism and Therapeutic Prospects

2018

Comp Rev Food Sci Food Safe

190

122

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“…Specific bile acids, such as deoxycholate and chenodeoxycholate, can stimulate intestinal chloride secretion 97, 98 which is accompanied by water. SCFAs, like bile acids, are important intraluminal determinants of mucus and water secretion through effects on sodium and water influx 99 , duodenal bicarbonate secretion 100 , and colonic epithelial 5-HT 3 receptor expression 101 .…”

Section: Effect Of the Gut Microbiota On Host Physiologymentioning

confidence: 99%

The Gut Microbiome in Adult and Pediatric Functional Gastrointestinal Disorders

Shin

Preidis

Shulman

et al. 2019

Clinical Gastroenterology and Hepatology

Self Cite

128

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The importance of gut microbiota in gastrointestinal (GI) physiology was well described, but our ability to study gut microbial ecosystems in their entirety was limited by culture-based methods prior to the sequencing revolution. The advent of high-throughput sequencing opened new avenues, allowing us to study gut microbial communities as an aggregate, independent of our ability to culture individual microbes. Early studies focused on association of changes in gut microbiota with different disease states, which was necessary to identify a potential role for microbes and generate novel hypotheses. Over the past few years the field has moved beyond associations to better understand the mechanistic implications of the microbiome in the pathophysiology of complex diseases. This movement also has resulted in a shift in our focus toward therapeutic strategies, which rely on better understanding the mediators of gut microbiota-host cross-talk. It is not surprising the gut microbiome has been implicated in the pathogenesis of functional gastrointestinal disorders given its role in modulating physiological processes such as immune development, GI motility and secretion, epithelial barrier integrity, and brain-gut communication. In this review, we focus on the current state of knowledge and future directions in microbiome research as it pertains to functional gastrointestinal disorders. We summarize the factors that help shape the gut microbiome in human beings. We discuss data from animal models and human studies to highlight existing paradigms regarding the mechanisms underlying microbiota-mediated alterations in physiological processes and their relevance in human interventions. While translation of microbiome science is still in its infancy, the outlook is optimistic and we are advancing in the right direction toward precise mechanism-based microbiota therapies.

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“…Bhattarai et al [62] analysed serotonin-sensitive ion secretion in GF mice in comparison with mice colonised with human gut microbiota, and showed that GF mice had a notably greater secretory response to serotonin than their human gut microbiota controls, indicating that the presence of gut microbiota may modulate the secretory response to 5-HT.…”

Section: Gut-microbiota and Serotonin Metabolismmentioning

confidence: 99%

The Relationship Between the Serotonin Metabolism, Gut-Microbiota and the Gut-Brain Axis

Stasi

Sadalla

Milani

2019

CDM

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Background:: Serotonin (5-HT) has a pleiotropic function in gastrointestinal, neurological/psychiatric and liver diseases. The aim of this review was to elucidate whether the gut-microbiota played a critical role in regulating peripheral serotonin levels. Methods:: We searched for relevant studies published in English using the PubMed database from 1993 to the present. Results: : Several studies suggested that alterations in the gut-microbiota may contribute to a modulation of serotonin signalling. The first indication regarded the changes in the composition of the commensal bacteria and the intestinal transit time caused by antibiotic treatment. The second indication regarded the changes in serotonin levels correlated to specific bacteria. The third indication regarded the fact that decreased serotonin transporter expression was associated with a shift in gut-microbiota from homeostasis to inflammatory type microbiota. Serotonin plays a key role in the regulation of visceral pain, secretion, and initiation of the peristaltic reflex; however, its altered levels are also detected in many different psychiatric disorders. Symptoms of some gastrointestinal functional disorders may be due to deregulation in central nervous system activity, dysregulation at the peripheral level (intestine), or a combination of both (brain-gut axis) by means of neuro-endocrine-immune stimuli. Moreover, several studies have demonstrated the profibrogenic role of 5-HT in the liver, showing that it works synergistically with platelet-derived growth factor in stimulating hepatic stellate cell proliferation. Conclusion:: Although the specific interaction mechanisms are still unclear, some studies have suggested that there is a correlation between the gut-microbiota, some gastrointestinal and liver diseases and the serotonin metabolism.

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Human-derived gut microbiota modulates colonic secretion in mice by regulating 5-HT₃ receptor expression via acetate production

Cited by 73 publications

References 39 publications

Dietary Amino Acids and the Gut‐Microbiome‐Immune Axis: Physiological Metabolism and Therapeutic Prospects

Dietary Amino Acids and the Gut‐Microbiome‐Immune Axis: Physiological Metabolism and Therapeutic Prospects

The Gut Microbiome in Adult and Pediatric Functional Gastrointestinal Disorders

The Relationship Between the Serotonin Metabolism, Gut-Microbiota and the Gut-Brain Axis

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Human-derived gut microbiota modulates colonic secretion in mice by regulating 5-HT3 receptor expression via acetate production

Cited by 73 publications

References 39 publications

Dietary Amino Acids and the Gut‐Microbiome‐Immune Axis: Physiological Metabolism and Therapeutic Prospects

Dietary Amino Acids and the Gut‐Microbiome‐Immune Axis: Physiological Metabolism and Therapeutic Prospects

The Gut Microbiome in Adult and Pediatric Functional Gastrointestinal Disorders

The Relationship Between the Serotonin Metabolism, Gut-Microbiota and the Gut-Brain Axis

Contact Info

Product

Resources

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Human-derived gut microbiota modulates colonic secretion in mice by regulating 5-HT₃ receptor expression via acetate production