Defining Dysbiosis in Inflammatory Bowel Disease

Jong, Renske J. de; Ohnmacht, Caspar

doi:10.1016/j.immuni.2018.12.028

Cited by 17 publications

(10 citation statements)

References 10 publications

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“…[6] Studies have suggested that development of IBD is closely related to the patients' autoimmune regulation, gene-microbiota interactions, and dietary factors. [7][8][9] Subsequent studies revealed that patients with IBD can show augmented T cell trans-differentiation in the intestine and blood. [10] Human orthologs, Atg16l1 and Nod2 genes, are also connected with an increased risk for developing IBD considering the defective induction of regulatory T cells (T-regs) to suppress mucosal inflammation.…”

Section: Introductionmentioning

confidence: 99%

An Insight into the Roles of Dietary Tryptophan and Its Metabolites in Intestinal Inflammation and Inflammatory Bowel Disease

Zhang

Zabed

et al. 2021

Molecular Nutrition Food Res

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Inflammatory bowel disease (IBD) is complex, chronic, and relapsing gastrointestinal inflammatory disorders, which includes mainly two conditions, namely ulcerative colitis (UC) and Crohn's disease (CD). Development of IBD in any individual is closely related to his/her autoimmune regulation, gene‐microbiota interactions, and dietary factors. Dietary tryptophan (Trp) is an essential amino acid for intestinal mucosal cells, and it is associated with the intestinal inflammation, epithelial barrier, and energy homeostasis of the host. According to recent studies, Trp and its three major metabolic pathways, namely kynurenine (KYN) pathway, indole pathway, and 5‐hydroxytryptamine (5‐HT) pathway, have vital roles in the regulation of intestinal inflammation by acting directly or indirectly on the pro/anti‐inflammatory cytokines, functions of various immune cells, as well as the intestinal microbial composition and homeostasis. In this review, recent advances in Trp‐ and its metabolites‐associated intestinal inflammation are summarized. It further discusses the complex mechanisms and interrelationships of the three major metabolic pathways of Trp in regulating inflammation, which could elucidate the value of dietary Trp to be used as a nutrient for IBD patients.

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Section: Introductionmentioning

confidence: 99%

An Insight into the Roles of Dietary Tryptophan and Its Metabolites in Intestinal Inflammation and Inflammatory Bowel Disease

Zhang

Zabed

et al. 2021

Molecular Nutrition Food Res

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“…The occurrence and development of UC are related to intestinal T cell dysfunction, mainly manifested as the imbalance of Th17/Treg cells [ 7 ]. Researchers found that the increase of Th17 cells in the lamina propria was accompanied by an altered structure of the intestinal crypts in UC patients [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Baicalein Restores the Balance of Th17/Treg Cells via Aryl Hydrocarbon Receptor to Attenuate Colitis

Liu

Chen

et al. 2020

Mediators of Inflammation

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As one of the ligands of aryl hydrocarbon receptor (AhR), baicalein, isolated from Scutellaria baicalensis Georgi, has been proved to exert potential therapeutic effects on ulcerative colitis (UC), but its therapeutic mechanism remains obscure. Authentically, ulcerative colitis can be alleviated by regulating the differentiation of naïve CD4+ T cells via AhR activation. So, our study planned to prove the hypothesis that baicalein protected mice against UC by regulating the balance of Th17/Treg cells via AhR activation. Immunofluorescence and western blot results showed that baicalein could promote AhR activation and induce it to transfer to the nucleus. We further determined the effect of baicalein on naïve CD4+ T cell differentiation in vitro by magnetic cell separation and drug intervention. The results showed that baicalein could promote Treg cell differentiation by activating AhR. In vivo study, UC mice were established by free drinking of dextran sulfate sodium (DSS) for 7 days and then were orally administrated by baicalein (10, 20, and 40 mg/kg), TCDD (AhR agonist), and CH223191 (antagonist). The results demonstrated that baicalein improved the symptoms of UC mice, regulated the balance of Th17/Treg cells, and restored the balance of proinflammatory cytokines such as IL-17, IL-6, and TNF-α; anti-inflammatory cytokines such as IL-10 and TGF-β; and epithelial protective cytokine IL-22 in UC mice, and these effects were related to AhR. Taken together, our research found that baicalein might be a potential drug for UC via regulating Treg cell differentiation and maintaining immune homeostasis and attempted to shed a light on the pivotal role of AhR in these effects.

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“…Impairment of this delicate ecosystem between the host and the microbiota may interfere with the development of the immune system. Its adverse quantitative and qualitative changes referred to as dysbiosis result in the development of pathological states [3][4][5][6][7]. The role of intestinal microbiota is still insufficiently understood, however, without any doubts there exists a tight relationship between dysbiosis of gut microbiota and disorders of other organ systems.…”

Section: Introductionmentioning

confidence: 99%

Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice

Gancarčíková

Lauko

Hrčková

et al. 2020

Cells

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The aim of this study was to investigate the use of a standardized animal model subjected to antibiotic treatment, and the effects of this treatment on the course of dextran sodium sulphate (DSS)-induced colitis in mice. By decontamination with selective antibiotics and observation of pathogenesis of ulcerative colitis (UC) induced chemically by exposure of mice to various concentrations of DSS, we obtained an optimum animal PGF model of acute UC manifested by mucin depletion, epithelial degeneration and necrosis, leading to the disappearance of epithelial cells, infiltration of lamina propria and submucosa with neutrophils, cryptitis, and accompanied by decreased viability of intestinal microbiota, loss of body weight, dehydration, moderate rectal bleeding, and a decrease in the selected markers of cellular proliferation and apoptosis. The obtained PGF model did not exhibit changes that could contribute to inflammation by means of alteration of the metabolic status and the induced dysbiosis did not serve as a bearer of pathogenic microorganisms participating in development of ulcerative colitis. The inflammatory process was induced particularly by exposure to DSS and its toxic action on compactness and integrity of mucosal barrier in the large intestine. This offers new possibilities of the use of this animal model in studies with or without participation of pathogenic microbiota in IBD pathogenesis.

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Defining Dysbiosis in Inflammatory Bowel Disease

Cited by 17 publications

References 10 publications

An Insight into the Roles of Dietary Tryptophan and Its Metabolites in Intestinal Inflammation and Inflammatory Bowel Disease

An Insight into the Roles of Dietary Tryptophan and Its Metabolites in Intestinal Inflammation and Inflammatory Bowel Disease

Baicalein Restores the Balance of Th17/Treg Cells via Aryl Hydrocarbon Receptor to Attenuate Colitis

Innovative Animal Model of DSS-Induced Ulcerative Colitis in Pseudo Germ-Free Mice

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