Darmflora als Regulator des Immunsystems

Chang, Hyun Dong; Kamradt, Thomas

doi:10.1007/s00393-011-0907-2

Cited by 3 publications

(2 citation statements)

References 10 publications

(7 reference statements)

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“…3,4 As a crucial part of the intestinal mucosal barrier, the mechanical barrier is mainly composed of intestinal epithelial cells and tight junction (TJ) proteins between cells 5,6 whose damage will cause the pathogenic bacteria and endotoxin to migrate into extraintestinal tissues, activate the immune system, and aggravate the inflammatory response. 7,8 Gut microbiota is essential for protecting the gut from injury, 9,10 and generally a stable intestinal microbiota structure may prevent inflammation by resisting the colonization of pathogenic bacteria. 11 Besides, recent studies showed that gut microbiota-derived metabolites could dramatically affect the immune balance and maintain the intestinal mucosal integrity.…”

Section: ■ Introductionmentioning

confidence: 99%

“…Gut microbiota is essential for protecting the gut from injury, , and generally a stable intestinal microbiota structure may prevent inflammation by resisting the colonization of pathogenic bacteria . Besides, recent studies showed that gut microbiota-derived metabolites could dramatically affect the immune balance and maintain the intestinal mucosal integrity .…”

Section: Introductionmentioning

confidence: 99%

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Theabrownin from Fu Brick Tea Improves Ulcerative Colitis by Shaping the Gut Microbiota and Modulating the Tryptophan Metabolism

Yang

Shao

et al. 2023

J. Agric. Food Chem.

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Fu brick tea theabrownin (FBTB) is a kind of biomacromolecule produced by oxidative polymerization of tea polyphenols. Although a variety of diseases can be alleviated by TB, its ability to treat ulcerative colitis (UC) is still worth exploring. A dextran sulfate sodium (DSS)-induced chronic UC mouse model was designed to first explore the alleviatory effect of FBTB on UC and its underlying mechanism by the sequencing of fecal 16S rRNA genes, metabolomics, and fecal microbiota transplantation (FMT). Administration of FBTB at 400 mg/kg bw in DSS-damaged mice could effectively reduce colonic damage and inflammation and improve colonic antioxidant capacity to relieve the UC-caused symptoms. FBTB could correct the disrupted gut microbiota caused by UC and contribute to the proliferation of Lactobacillus and Parasutterella. FMT in combination with antibiotic treatment showed that FBTB could elevate the levels of microbial tryptophan metabolites, including indole-3-acetaldehyde (IAld) and indole-3-acetic acid (IAA), by selectively promoting the growth of Lactobacillus. Importantly, FBTB-elevated IAld and IAA could activate aromatic hydrocarbon receptors (AhRs) and enhance interleukin-22 production to repair the intestinal barrier. These findings demonstrated that FBTB alleviated UC mainly by targeting the gut microbiota involved in the AhR pathway for prophylactic and therapeutic treatment of UC.

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