Impact of Proinflammatory Cytokines and Mesalamine on the Expression of the Tight Junction Protein Claudin-1 in Intestinal Epithelial Cells

Weber, Lisa-Maria; Fischer, Andréas; Scholz, Saskia; Metzke, Diana; Baumgart, Daniel C.

doi:10.1016/s0016-5085(17)32573-8

Cited by 5 publications

(4 citation statements)

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“…Evidence from clinical trials indicated that impaired intestinal barrier is connected with occurrence and development of UC [41,42]. Occludin and claudin-1 as the major tight junction proteins constitute the basic structure of tight junctions in intestinal barrier [43][44][45]. Myosin light chain kinase (MLCK) is also a key effecter of barrier dysfunction and a potential therapeutic target [46].…”

Section: Discussionmentioning

confidence: 99%

Bu-Zhong-Yi-Qi Granule Enhances Colonic Tight Junction Integrity via TLR4/NF-κB/MLCK Signaling Pathway in Ulcerative Colitis Rats

Kang

Jia

Zhao

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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Background. Bu-zhong-yi-qi granule (BZYQ), a sort of Chinese herbal medicine, has exhibited therapeutic effects on ulcerative colitis (UC). However, the mechanism of BZYQ has not been fully clarified. This study was aimed at investigating the effects of BZYQ on UC rats model and at exploring its potential mechanism. Methods. The UC rats were established by enema of trinitrobenzene sulfonic acid (TNBS). The therapeutic effects of BZYQ treatment were evaluated by disease activity index (DAI), colon macroscopic damage index (CMDI) scores, and histological observation. The mRNA levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-10 (IL-10) were measured by quantitative real time-polymerase chain reaction (qPCR). The expression of tight junction (TJ) proteins, occludin and claudin-1, in the colon was determined by Western blot and immunofluorescence. The expression of toll-like receptors 4 (TLR4), nuclear factor-kappa B (NF-κB), p-NF-κB, myosin light chain kinase (MLCK), MLC, and p-MLC levels in colon was determined by Western blot or qPCR. Results. The results showed that BZYQ could attenuate DAI, CMDI, and histological inflammation. TJ proteins expression was decreased in UC rats, but treatment with BZYQ restored the expression of occludin and claudin-1. In addition, BZYQ administration ameliorated UC-associated increase in the production of TNF-α, IL-1β, and the expression of TLR4, NF-κB, p-NF-κB, MLCK, MLC, and p-MLC, while BZYQ administration increased the production of IL-10. Conclusions. The therapeutic effect of BZYQ on UC is at least partially through regulation of the secretion of some inflammatory cytokines and improvement of TJ integrity via TLR4/NF-κB/MLCK pathway.

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Section: Discussionmentioning

confidence: 99%

Bu-Zhong-Yi-Qi Granule Enhances Colonic Tight Junction Integrity via TLR4/NF-κB/MLCK Signaling Pathway in Ulcerative Colitis Rats

Kang

Jia

Zhao

et al. 2021

Evidence-Based Complementary and Alternative Medicine

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“…Therefore, a vicious cycle of mucosal barrier dysfunction and inflammation is established. 48,49 barrier. 50 The CLNA1, CLNA2, and CLNA mixture significantly upregulated TJ proteins (E-cadherin 1, ZO-1, claudin-3, and occludin), and CLNA1 showed a stronger role in protecting the intestinal barrier than PA. Lactobacillusderived CLNA also manifested stronger regulation of the expression of relative cytokines than PA. As for the level of cytokine, PA just showed significance on IL-6, but Lactobacillus-derived CLNA showed significance on IL-β, TNF-α, and PPARγ.…”

Section: ■ Discussionmentioning

confidence: 99%

“…The alteration in cytokine profiles, in turn, further triggers the decline in tight junctions. Therefore, a vicious cycle of mucosal barrier dysfunction and inflammation is established. , Treatments with Lactobacillus -derived CLNAs increased the concentration of MUC2, contributing to the integrity of the colonic mucus layer and goblet cells. Tight junction proteins connect enterocytes and play an important role in the integrity of the intestinal barrier .…”

Section: Discussionmentioning

confidence: 99%

c9, t11, c15-CLNA and t9, t11, c15-CLNA from Lactobacillus plantarum ZS2058 Ameliorate Dextran Sodium Sulfate-Induced Colitis in Mice

Ren

Yang

Zhang

et al. 2020

J. Agric. Food Chem.

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To investigate the specific functions of conjugated fatty acids (CFAs) produced by the probiotic bacterium, α-linolenic acid was isomerized by Lactobacillus plantarum ZS2058, and two different conjugated linolenic acid (CLNA) isomers were successfully isolated: c9, t11, c15-CLNA (CLNA1) and t9, t11, c15-CLNA (CLNA2). The effects and mechanism of CLNA crude extract and individual isomers on colitis were explored. CLNA significantly inhibited weight loss, the disease activity index, and colon shortening. Additionally, CLNA alleviated histological damage, protected colonic mucus layer integrity, and significantly upregulated the concentration of tight junction proteins (ZO-1, occludin, E-cadherin 1, and claudin-3). CLNA significantly attenuated the level of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) while upregulating the expression of the colonic anti-inflammatory cytokine IL-10 and nuclear receptor peroxisome-activated receptor-γ. Moreover, CLNA increased the activity of oxidative stress-related enzymes (SOD, GSH, and CAT), and the myeloperoxidase activity was significantly decreased by CLNA. Meanwhile, the concentrations of CLNA in the liver and conjugated linoleic acid in the colonic content were significantly increased because of the treatment of CLNA. Furthermore, CLNA could rebalance the intestinal microbial composition of colitis mice, including increasing the α-diversity. CLNA1 and CLNA2 increased the abundance of Ruminococcus and Prevotella, respectively.

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“…In IBD, the intestinal permeability of the patient's intestinal mucosa increases, and the expression of the tight junction protein (TJP) decreases, which affects the protective function of the intestine and causes inflammation [87]. Inflammation of the intestinal epithelial mucosa will exacerbate this phenomenon, leading to a further decrease in TJP and forming a vicious circle [88]. Studies have shown that feeding mice with B. longum YS108R can improve the mucosal barrier damage induced by DSS and increase the expression of TJP and mucin2 to alleviate colitis [24].…”

Section: Bifidobacterium Longum Enhances the Intestinal Barriermentioning

confidence: 99%

Bifidobacterium Longum: Protection against Inflammatory Bowel Disease

Yao

Zhao

Wang

et al. 2021

Journal of Immunology Research

130

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The prevalence of inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn’s disease (CD), increases gradually worldwide in the past decades. IBD is generally associated with the change of the immune system and gut microbiota, and the conventional treatments usually result in some side effects. Bifidobacterium longum, as colonizing bacteria in the intestine, has been demonstrated to be capable of relieving colitis in mice and can be employed as an alternative or auxiliary way for treating IBD. Here, the mechanisms of the Bifidobacterium longum in the treatment of IBD were summarized based on previous cell and animal studies and clinical trials testing bacterial therapies. This review will be served as a basis for future research on IBD treatment.

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Impact of Proinflammatory Cytokines and Mesalamine on the Expression of the Tight Junction Protein Claudin-1 in Intestinal Epithelial Cells

Cited by 5 publications

References 0 publications

Bu-Zhong-Yi-Qi Granule Enhances Colonic Tight Junction Integrity via TLR4/NF-κB/MLCK Signaling Pathway in Ulcerative Colitis Rats

Bu-Zhong-Yi-Qi Granule Enhances Colonic Tight Junction Integrity via TLR4/NF-κB/MLCK Signaling Pathway in Ulcerative Colitis Rats

c9, t11, c15-CLNA and t9, t11, c15-CLNA from Lactobacillus plantarum ZS2058 Ameliorate Dextran Sodium Sulfate-Induced Colitis in Mice

Bifidobacterium Longum: Protection against Inflammatory Bowel Disease

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