Gut microbiota-dependent catabolites of tryptophan play a predominant role in the protective effects of Turmeric polysaccharides against DSS-induced ulcerative colitis

Alterations in the gut microbiota composition and diversity seem to play a role in the development of chronic diseases, including inflammatory bowel disease (IBD), leading to gut barrier disruption and induction of proinflammatory immune responses. This opens the door for the use of novel health-promoting bacteria. We selected five Parabacteroides distasonis strains isolated from human adult and neonates gut microbiota. We evaluated in vitro their immunomodulation capacities and their ability to reinforce the gut barrier and characterized in vivo their protective effects in an acute murine model of colitis. The in vitro beneficial activities were highly strain dependent: two strains exhibited a potent anti-inflammatory potential and restored the gut barrier while a third strain reinstated the epithelial barrier. While their survival to in vitro gastric conditions was variable, the levels of P. distasonis DNA were higher in the stools of bacteria-treated animals. The strains that were positively scored in vitro displayed a strong ability to rescue mice from colitis. We further showed that two strains primed dendritic cells to induce regulatory T lymphocytes from naïve CD4+ T cells. This study provides better insights on the functionality of commensal bacteria and crucial clues to design live biotherapeutics able to target inflammatory chronic diseases such as IBD.

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Altered Gut Microbiota in Patients With Chronic Pancreatitis is Associated With Gut Barrier Dysfunction and Metabolic Abnormalities

Clinical Gastroenterology and Hepatology ◽

10.1016/j.cgh.2016.09.023 ◽

2017 ◽

Vol 15 (1) ◽

pp. 153

Author(s):

Rupjyoti Talukdar ◽

S.M. Jandhyala ◽

R. Reddy ◽

M. Arutla ◽

D.N. Reddy

Keyword(s):

Chronic Pancreatitis ◽

Gut Microbiota ◽

Metabolic Abnormalities ◽

Barrier Dysfunction ◽

Gut Barrier

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Qing-Re-Xiao-Zheng Formula Modulates Gut Microbiota and Inhibits Inflammation in Mice With Diabetic Kidney Disease

Frontiers in Medicine ◽

10.3389/fmed.2021.719950 ◽

2021 ◽

Vol 8 ◽

Author(s):

Yabin Gao ◽

Ruibing Yang ◽

Lan Guo ◽

Yaoxian Wang ◽

Wei Jing Liu ◽

...

Keyword(s):

Kidney Disease ◽

Gut Microbiota ◽

Diabetic Kidney Disease ◽

Inflammatory Responses ◽

Protective Effects ◽

Mice Model ◽

Diabetic Kidney ◽

Metabolic Inflammation ◽

Gut Microbiota Dysbiosis

Evidence indicates that the metabolic inflammation induced by gut microbiota dysbiosis contributes to diabetic kidney disease. Prebiotic supplementations to prevent gut microbiota dysbiosis, inhibit inflammatory responses, and protect the renal function in DKD. Qing-Re-Xiao-Zheng formula (QRXZF) is a Traditional Chinese Medicine (TCM) formula that has been used for DKD treatment in China. Recently, there are growing studies show that regulation of gut microbiota is a potential therapeutic strategy for DKD as it is able to reduce metabolic inflammation associated with DKD. However, it is unknown whether QRXZF is effective for DKD by regulating of gut microbiota. In this study, we investigated the reno-protective effect of QRXZF by exploring its potential mechanism between gut microbiota and downstream inflammatory pathways mediated by gut-derived lipopolysaccharide (LPS) in the kidney. High-fat diet (HFD) and streptozotocin injection-induced DKD mice model was established to assess the QRXZF effect in vivo. Mice treated with QRXZF for 8 weeks had significantly lower levels of urinary albumin, serum cholesterol and triglycerides. The renal injuries observed through histological analysis were attenuated as well. Also, mice in the QRXZF group had higher levels of Zonula occludens protein-1 (ZO-1) expression, lower levels of serum fluorescein-isothiocyanate (FITC)-dextran and less-damaged colonic mucosa as compared to the DKD group, implying the benefit role for the gut barrier integrity. QRXZF treatment also reversed gut dysbiosis and reduced levels of gut-derived LPS. Notably, the expression of toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB), which are important inflammation pathways in DKD, were suppressed in the QRXZF groups. In conclusion, our results indicated that the reno-protective effects of QRXZF was probably associated with modulating gut microbiota and inhibiting inflammatory responses in the kidney.

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Fermentation Supernatants of Pleurotus eryngii Mushroom Ameliorate Intestinal Epithelial Barrier Dysfunction in Lipopolysaccharide-Induced Caco-2 Cells via Upregulation of Tight Junctions

Microorganisms ◽

10.3390/microorganisms9102071 ◽

2021 ◽

Vol 9 (10) ◽

pp. 2071

Author(s):

Georgia Saxami ◽

Evangelia N. Kerezoudi ◽

Evdokia K. Mitsou ◽

Georgios Koutrotsios ◽

Georgios I. Zervakis ◽

...

Keyword(s):

Gene Expression ◽

Gut Microbiota ◽

Tight Junctions ◽

Pleurotus Eryngii ◽

Protective Effects ◽

Barrier Dysfunction ◽

Carbohydrate Source ◽

Expression Levels ◽

Vitro Effect

In recent years, modulation of gut microbiota through prebiotics has garnered interest as a potential to ameliorate intestinal barrier dysfunction. The aim of the study was to examine the in vitro effect of fermentation supernatants (FSs) from rich in β-glucan Pleurotus eryngii mushrooms on the expression levels of tight junctions (TJs) genes in Caco-2 cells stimulated by bacterial lipopolysaccharides (LPS). Mushrooms were fermented using fecal inocula in an in vitro batch culture model. Caco-2 cells were subjected to LPS and FS treatment under three different conditions: pre-incubation with FS, co- and post-incubation. Reverse transcription PCR was applied to measure the expression levels of zonulin-1, occludin and claudin-1 genes. FSs from P. eryngii mushrooms led to a significant upregulation of the TJs gene expression in pre-incubation state, indicating potential preventive action. Down-regulation of all TJs gene expression levels was observed when the cells were challenged with LPS. The FS negative control (gut microbiota of each donor with no carbohydrate source) exhibited a significant upregulation of TJs expression levels compared to the cells that were challenged with LPS, for all three conditions. Overall, our data highlighted the positive and potential protective effects of P. eryngii mushrooms in upregulation of TJs’ genes.

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Metformin Exerts Anti-inflammatory and Mucus Barrier Protective Effects by Enriching Akkermansia muciniphila in Mice With Ulcerative Colitis

Frontiers in Pharmacology ◽

10.3389/fphar.2021.726707 ◽

2021 ◽

Vol 12 ◽

Author(s):

Haoran Ke ◽

Fang Li ◽

Wenlin Deng ◽

Zitong Li ◽

Siqi Wang ◽

...

Keyword(s):

Ulcerative Colitis ◽

Gut Microbiota ◽

Treated Group ◽

Protective Effects ◽

Microbiota Composition ◽

16S Rrna Analysis ◽

Akkermansia Muciniphila ◽

Anti Inflammatory ◽

Mucus Barrier ◽

Gut Microbiota Composition

The present study aimed to determine if metformin exerts anti-inflammatory and mucus-protective effects via the gut microbiota. Metformin has extensive benefits including anti-inflammatory effects. Previous studies showed that metformin changed the gut microbiota composition and increases the number of goblet cells. Intestinal dysbiosis and goblet cell depletion are important features of ulcerative colitis (UC). The underlying mechanism and whether metformin can improve the mucus barrier in UC remain unclear. Metformin (400 mg/kg/day) was administered to mice with dextran sulfate sodium (DSS)-induced UC for 2 wk to investigate the effects of metformin on the intestinal mucus barrier. The gut microbiota was depleted, using antibiotics, to explore its role in the mucus-protecting effects of metformin. Akkermansia muciniphila (A. muciniphila), which was enriched in metformin-treated mice, was administered to mice to investigate the effects of the bacteria on UC and the mucus barrier. Metformin attenuated DSS-induced UC in mice, as evidenced by the alleviation of diarrhea, hematochezia, and the decrease in body weight. The expression of mucin2, a prominent mucus barrier protein, was increased in the metformin-treated group compared to the DSS-treated group. Furthermore, fecal 16S rRNA analysis showed that metformin treatment changed the gut microbiota composition by increasing the relative abundance of Lactobacillus and Akkermansia species while decreasing Erysipelatoclostridium at the genus level. Antibiotic treatment partly abolished the anti-inflammatory and mucus-protecting effects of metformin. Administration of A. muciniphila alleviated the colonic inflammation and mucus barrier disruption. Metformin alleviated DSS-induced UC in mice and protected against cell damage via affecting the gut microbiota, thereby providing a new mechanism for the therapeutic effect of metformin in patients with UC. This study also provides evidence that A. muciniphila as a probiotic has potential benefits for UC.

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Toxic effects of copper on jejunum and colon of pigs: mechanisms related to gut barrier dysfunction and inflammation influenced by gut microbiota

Food & Function ◽

10.1039/d1fo01286j ◽

2021 ◽

Author(s):

Jianzhao Liao ◽

Quanwei Li ◽

Chaiqin Lei ◽

Wenlan Yu ◽

Jichang Deng ◽

...

Keyword(s):

Gut Microbiota ◽

Toxic Effects ◽

Barrier Dysfunction ◽

Gut Barrier ◽

Trace Mineral ◽

Excessive Intake ◽

Host Physiology ◽

Mammalian Intestine

Copper (Cu) is an essential trace mineral, but the excessive intake can lead to potentially toxic effects on host physiology. The mammalian intestine harbors various microorganisms, which are associated with intestinal...

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Protective effects of tryptophan-catabolizing Lactobacillus plantarum KLDS 1.0386 against dextran sodium sulfate-induced colitis in mice

Food & Function ◽

10.1039/d0fo02622k ◽

2020 ◽

Vol 11 (12) ◽

pp. 10736-10747

Author(s):

Jialu Shi ◽

Peng Du ◽

Qinggang Xie ◽

Nana Wang ◽

Huizhen Li ◽

...

Keyword(s):

Ulcerative Colitis ◽

Acetic Acid ◽

Gut Microbiota ◽

Lactobacillus Plantarum ◽

Sodium Sulfate ◽

Dextran Sodium Sulfate ◽

Protective Effects ◽

Stat3 Signaling ◽

Stat3 Signaling Pathway ◽

Indole 3 Acetic Acid

L. plantarum KLDS 1.0386 combined with tryptophan alleviates ulcerative colitis (UC) induced by dextran sodium sulfate (DSS) by increasing the level of indole-3-acetic acid (IAA), stimulating the AHR/IL-22/STAT3 signaling pathway and regulating gut microbiota in mice.

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