Mucosal permeability is an intrinsic factor in susceptibility to dextran sulfate sodium-induced colitis in rats

Iwaya, Hitoshi; Maeta, Koushi; Hara, Hiroshi; Ishizuka, Satoshi

doi:10.1258/ebm.2011.011269

Cited by 17 publications

(19 citation statements)

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“…Consequently, translocation of ZO-1 and thereby the associated contraction of cytoskeletal actin is thought to play an important role in the regulation of epithelial barrier function (Umeda et al, 2006). We did not observe LPS-dependent effects on the total protein level of different tight junction proteins, such as ZO-1, occludin and claudin-1, but it is known that it is mainly not the expression level but the expression pattern of tight junction proteins that determines epithelial permeability (Iwaya et al, 2012). Not only the epithelial cell layer itself, but also the overlying mucus barrier, which consists of large glycoproteins called mucins, is extremely important for the intestinal barrier function.…”

Section: Discussionmentioning

confidence: 59%

Bacteroides uniformis CECT 7771 Ameliorates Metabolic and Immunological Dysfunction in Mice with High-Fat-Diet Induced Obesity

2014

Health and the Gut

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Several pathological processes, such as sepsis and inflammatory bowel disease (IBD), are associated with impairment of intestinal epithelial barrier. Here, we investigated the role of matrix metalloproteinase MMP13 in these diseases. We observed that MMP13 À/À mice display a strong protection in LPS-and caecal ligation and puncture-induced sepsis. We could attribute this protection to reduced LPS-induced goblet cell depletion, endoplasmic reticulum stress, permeability and tight junction destabilization in the gut of MMP13 À/À mice compared to MMP13 þ/þ mice. Both in vitro and in vivo, we found that MMP13 is able to cleave pro-TNF into bioactive TNF. By LC-MS/MS, we identified three MMP13 cleavage sites, which proves that MMP13 is an alternative TNF sheddase next to the TNF converting enzyme TACE. Similarly, we found that the same mechanism was responsible for the observed protection of the MMP13mice in a mouse model of DSS-induced colitis. We identified MMP13 as an important mediator in sepsis and IBD via the shedding of TNF. Hence, we propose MMP13 as a novel drug target for diseases in which damage to the gut is essential.

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Section: Discussionmentioning

confidence: 59%

Bacteroides uniformis CECT 7771 Ameliorates Metabolic and Immunological Dysfunction in Mice with High-Fat-Diet Induced Obesity

2014

Health and the Gut

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“…Dietary Dex possibly affected the population and functions of immune cells. We previously demonstrated that IFN-γ mRNA expression did not increase in early phase of DSS-induced colitis in an inbred strain originated from Wistar strain [39]. In contrast, IL-1β mRNA expression increased even in the early phase of the colitis.…”

Section: Discussionmentioning

confidence: 91%

The Delay in the Development of Experimental Colitis from Isomaltosyloligosaccharides in Rats Is Dependent on the Degree of Polymerization

et al. 2012

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BackgroundIsomaltosyloligosaccharides (IMO) and dextran (Dex) are hardly digestible in the small intestine and thus influence the luminal environment and affect the maintenance of health. There is wide variation in the degree of polymerization (DP) in Dex and IMO (short-sized IMO, S-IMO; long-sized IMO, L-IMO), and the physiological influence of these compounds may be dependent on their DP.Methodology/Principal FindingsFive-week-old male Wistar rats were given a semi-purified diet with or without 30 g/kg diet of the S-IMO (DP = 3.3), L-IMO (DP = 8.4), or Dex (DP = 1230) for two weeks. Dextran sulfate sodium (DSS) was administered to the rats for one week to induce experimental colitis. We evaluated the clinical symptoms during the DSS treatment period by scoring the body weight loss, stool consistency, and rectal bleeding. The development of colitis induced by DSS was delayed in the rats fed S-IMO and Dex diets. The DSS treatment promoted an accumulation of neutrophils in the colonic mucosa in the rats fed the control, S-IMO, and L-IMO diets, as assessed by a measurement of myeloperoxidase (MPO) activity. In contrast, no increase in MPO activity was observed in the Dex-diet-fed rats even with DSS treatment. Immune cell populations in peripheral blood were also modified by the DP of ingested saccharides. Dietary S-IMO increased the concentration of n-butyric acid in the cecal contents and the levels of glucagon-like peptide-2 in the colonic mucosa.Conclusion/SignificanceOur study provided evidence that the physiological effects of α-glucosaccharides on colitis depend on their DP, linkage type, and digestibility.

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“…Previous reports have demonstrated that DSS treatment impairs the TJ barrier and/or structure of the rat colon and intestinal Caco-2 cells (26,27), indicating the direct effect of DSS on intestinal epithelial cells. DSS is thought to influence the signaling pathways leading to TJ barrier regulation in epithelial cells, as the expression and localization of TJ proteins are regulated by various signaling pathways.…”

Section: Discussionmentioning

confidence: 93%

Supplemental Naringenin Prevents Intestinal Barrier Defects and Inflammation in Colitic Mice

Azuma

Shigeshiro

Kodama³

et al. 2013

The Journal of Nutrition

134

108

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Intestinal barrier defects are involved in the pathogenesis of inflammatory bowel disease. The present study investigated the ameliorative effects of naringenin, a citrus polyphenol, on intestinal tight junction (TJ) barrier defects and inflammation in a murine model of colitis. In Expt. 1, using a 2 × 2 fractional design, the mice were administered water or 2% dextran sulfate sodium (DSS) in combination with feeding control or naringenin-containing diets for 9 d (severe disease stage). DSS administration caused severe colon damage and inflammation, as indicated by body weight loss, increased clinical sores, colon shortening, and gene expressions of inflammatory cytokines [interferon-γ, interleukin (IL)-6, macrophage inflammatory protein-2, and IL-17A). DSS administration also impaired TJ barrier integrity in the colon, as indicated by increased colon permeability and plasma LPS-binding protein levels, resulting from the impaired colonic expression of TJ proteins, occludin, junctional adhesion molecule-A, and claudin-3. Supplemental feeding with naringenin totally or partially attenuated these symptoms, suggesting that naringenin ameliorates the DSS-induced colitis at least partially through protection of the TJ barrier. In Expt. 2, analyses were performed at different disease stages (d 3, 6, and 9) to more widely examine the ameliorative role of naringenin on the initiation and development of colitis. DSS administration moderately induced colon shortening at d 3 and 6 and increased the disease activity index (DAI) and inflammatory cytokine (IL-6 and IL-17A) expression without any significant increases in colonic permeability. Feeding naringenin attenuated the increased DAI and colon shortening and tended to suppress the increased cytokine expression. These findings suggest that the presence of an additional mechanism underlying the naringenin-mediated, anticolitic effect along with barrier protection.

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Mucosal permeability is an intrinsic factor in susceptibility to dextran sulfate sodium-induced colitis in rats

Cited by 17 publications

References 50 publications

Bacteroides uniformis CECT 7771 Ameliorates Metabolic and Immunological Dysfunction in Mice with High-Fat-Diet Induced Obesity

Bacteroides uniformis CECT 7771 Ameliorates Metabolic and Immunological Dysfunction in Mice with High-Fat-Diet Induced Obesity

The Delay in the Development of Experimental Colitis from Isomaltosyloligosaccharides in Rats Is Dependent on the Degree of Polymerization

Supplemental Naringenin Prevents Intestinal Barrier Defects and Inflammation in Colitic Mice

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