The Interplay between Nutrition, Innate Immunity, and the Commensal Microbiota in Adaptive Intestinal Morphogenesis

Bayer, Franziska; Dremova, Olga; Khuu, My Phung; Mammadova, Könül; Pontarollo, Giulia; Kiouptsi, Klytaimnistra; Soshnikova, Natalia; May-Simera, Helen; Reinhardt, Carsten

doi:10.3390/nu13072198

Cited by 17 publications

(8 citation statements)

References 303 publications

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“…Besides, the anatomy of the GI tract shows remarkable flexibility to gut microbial challenges in adults. The interaction of gut microbiota with innate immune cells and pattern recognition receptors regulates cellular and morphologic properties of the GI tract, including the renewal and differentiation of the epithelial lineage, the adaptation of the intestinal microvasculature, and the shape of the ENS and the intestinal smooth muscle layers (21). The ENS is an intrinsic neuronal network that harbors various types of nerve cells located along the GI tract, which not only controls GI motility, fluid homeostasis, and blood flow but also interacts with epithelial and immune cells in the intestine (13).…”

Section: Introductionmentioning

confidence: 99%

Role of gut microbiota-derived signals in the regulation of gastrointestinal motility

Zheng

Tang

et al. 2022

Front. Med.

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The gastrointestinal (GI) tract harbors trillions of commensal microbes, called the gut microbiota, which plays a significant role in the regulation of GI physiology, particularly GI motility. The GI tract expresses an array of receptors, such as toll-like receptors (TLRs), G-protein coupled receptors, aryl hydrocarbon receptor (AhR), and ligand-gated ion channels, that sense different gut microbiota-derived bioactive substances. Specifically, microbial cell wall components and metabolites, including lipopeptides, peptidoglycan, lipopolysaccharides (LPS), bile acids (BAs), short-chain fatty acids (SCFAs), and tryptophan metabolites, mediate the effect of gut microbiota on GI motility through their close interactions with the enteroendocrine system, enteric nervous system, intestinal smooth muscle, and immune system. In turn, GI motility affects the colonization within the gut microbiota. However, the mechanisms by which gut microbiota interacts with GI motility remain to be elucidated. Deciphering the underlying mechanisms is greatly important for the prevention or treatment of GI dysmotility, which is a complication associated with many GI diseases, such as irritable bowel syndrome (IBS) and constipation. In this perspective, we overview the current knowledge on the role of gut microbiota and its metabolites in the regulation of GI motility, highlighting the potential mechanisms, in an attempt to provide valuable clues for the development of gut microbiota-dependent therapy to improve GI motility.

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Section: Introductionmentioning

confidence: 99%

Role of gut microbiota-derived signals in the regulation of gastrointestinal motility

Zheng

Tang

et al. 2022

Front. Med.

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“…For this reason, organisms have to be viewed as holobionts, including their microbiota affecting many organ systems (Meyer-Albich 1950 ; Margulis and Fester 1991 ). This is not only exemplified by the evoked adaptive changes in gut morphology or by recent studies on the gut-liver or gut-brain axis (Bayer et al 2021 ; de Vadder et al 2018 ; Formes et al 2021 ; Aswendt et al 2021 ), but also by the role of microbiota and its derived metabolites in cardiovascular disease (Karbach et al 2016 ).…”

Section: Introductionmentioning

confidence: 95%

Microbiota-derived tryptophan metabolites in vascular inflammation and cardiovascular disease

et al. 2022

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The essential amino acid tryptophan (Trp) is metabolized by gut commensals, yielding in compounds that affect innate immune cell functions directly, but also acting on the aryl hydrocarbon receptor (AHR), thus regulating the maintenance of group 3 innate lymphoid cells (ILCs), promoting T helper 17 (TH17) cell differentiation, and interleukin-22 production. In addition, microbiota-derived Trp metabolites have direct effects on the vascular endothelium, thus influencing the development of vascular inflammatory phenotypes. Indoxyl sulfate was demonstrated to promote vascular inflammation, whereas indole-3-propionic acid and indole-3-aldehyde had protective roles. Furthermore, there is increasing evidence for a contributory role of microbiota-derived indole-derivatives in blood pressure regulation and hypertension. Interestingly, there are indications for a role of the kynurenine pathway in atherosclerotic lesion development. Here, we provide an overview on the emerging role of gut commensals in the modulation of Trp metabolism and its influence in cardiovascular disease development.

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“…The major functions of the small intestine are food digestion, absorption and immune response to micro‐organisms 1 . All these physiological functions of the small intestine are regulated by its hormones 2 .…”

Section: Introductionmentioning

confidence: 99%

“…The major functions of the small intestine are food digestion, absorption and immune response to microorganisms. 1 All these physiological functions of the small intestine are regulated by its hormones. 2 Intestinal hormones are produced by enteroendocrine cells (EECs), which are located throughout the gastrointestinal tract and are highly variable in their morphology and gene expression patterns.…”

Section: Introductionmentioning

confidence: 99%

ID2 controls differentiation of enteroendocrine cells in mouse small intestine

et al. 2022

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Aims:The mammalian gut is the largest endocrine organ. Dozens of hormones secreted by enteroendocrine cells regulate a variety of physiological functions of the gut but also of the pancreas and brain. Here, we examined the role of the helix-loop-helix transcription factor ID2 during the differentiation of intestinal stem cells along the enteroendocrine lineage. Methods:To assess the functions of ID2 in the adult mouse small intestine, we used single-cell RNA sequencing, genetically modified mice, and organoid assays. Results:We found that in the adult intestinal epithelium Id2 is predominantly expressed in enterochromaffin and peptidergic enteroendocrine cells.Consistently, the loss of Id2 leads to the reduction of Chromogranin A-positive enteroendocrine cells. In contrast, the numbers of tuft cells are increased in Id2 mutant small intestine. Moreover, ablation of Id2 elevates the numbers of Serotonin + enterochromaffin cells and Ghrelin + X-cells in the posterior part of the small intestine. Finally, ID2 acts downstream of BMP signalling during the differentiation of Glucagon-like peptide-1 + L-cells and Cholecystokinin + I-cells towards Neurotensin + PYY + N-cells. Conclusion: ID2 plays an important role in cell fate decisions in the adult small intestine. First, ID2 is essential for establishing a differentiation gradient for enterochromaffin and X-cells along the anterior-posterior axis of the gut. Next, ID2 is necessary for the differentiation of N-cells thus ensuring a differentiation gradient along the crypt-villi axis. Finally, ID2 suppresses the commitment of secretory intestinal epithelial progenitors towards tuft cell lineage and thus controls host immune response to commensal and parasitic microbiota.

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The Interplay between Nutrition, Innate Immunity, and the Commensal Microbiota in Adaptive Intestinal Morphogenesis

Cited by 17 publications

References 303 publications

Role of gut microbiota-derived signals in the regulation of gastrointestinal motility

Role of gut microbiota-derived signals in the regulation of gastrointestinal motility

Microbiota-derived tryptophan metabolites in vascular inflammation and cardiovascular disease

ID2 controls differentiation of enteroendocrine cells in mouse small intestine

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