Adherent-Invasive Escherichia coli Induce Claudin-2 Expression and Barrier Defect in CEABAC10 Mice and Crohnʼs Disease Patients§

Denizot, Jérémy; Sivignon, Adeline; Barreau, Frédérick; Darcha, Claude; Chan, Carlos; Stanners, Clifford P.; Hofman, Paul; Darfeuille‐Michaud, Arlette; Barnich, Nicolas

doi:10.1002/ibd.21787

Cited by 84 publications

(69 citation statements)

References 51 publications

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“…Interestingly, other pathogenic bacteria, such as L. monocytogenes, S. typhimurium, Clostridium difficile, and some E. coli may also alter epithelial barrier function (33)(34)(35)(36)(37). However, the involved mechanisms differ from those described herein for Y. pseudotuberculosis.…”

Section: Discussionmentioning

confidence: 70%

“…L. monocytogenes increases paracellular permeability through a mechanism involving calcium influx (33,34,39). The adherent-invasive E. coli LF82 strain induces claudin-2 expression and a barrier defect in mice (37). Finally, enteropathogenic E. coli alters the epithelial TJ barrier through intracellular Ca 2+ changes and MLCK phosphorylation (39).…”

Section: Discussionmentioning

confidence: 99%

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Yersinia pseudotuberculosis disrupts intestinal barrier integrity through hematopoietic TLR-2 signaling

Jung¹,

Meinzer²,

Montcuquet³

et al. 2012

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Yersinia pseudotuberculosis disrupts intestinal barrier integrity through hematopoietic TLR-2 signaling

Jung¹,

Meinzer²,

Montcuquet³

et al. 2012

J. Clin. Invest.

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“…Intestinal barrier function was performed in control and P-80 fed mice using FITC-labeled dextran as previously described by Denizot, et al [11]. Mice were fasted overnight and then gavaged with 15 mg of FITC-labeled dextran 4kD (Sigma).…”

Section: In-vivo Permeabilitymentioning

confidence: 99%

Food Additive P-80 Impacts Mouse Gut Microbiota Promoting Intestinal Inflammation, Obesity and Liver Dysfunction

Singh¹

2016

SOJMID

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Open Access Research Articlethe globalization of unhealthy lifestyle. Key metabolic and physiological changes, including obesity, metabolic syndrome and Nonalcoholic Fatty Liver Disease (NAFLD) are commonly associated with chronic, non-communicable disease that are responsible for approximately 70% of the world's death.There are compelling arguments to include the composition of gut microbiota as a key risk factor for the development of obesity and obesity related metabolic disorders, including insulin resistance, type 2 diabetes, dyslipidemia and non-alcoholic fatty liver disease [3]. The gut microbiota has been implicated in having both direct (i.e. through effect on nutrient uptake) and indirect effect on health [4,5]. In mice, food additives have been demonstrated to affect the host microbiota interaction, leading to low-grade inflammation, adiposity and adiposity associated metabolic effect [6].We set out to elucidate whether alteration in the gut microbial community after P-80 ingestion is a causative agent of liver dysfunction. To explore this possibility, we setup an experiment to examine the impact of P-80 on gut microbiota using wild-type C57BL/ 6 mice. The experimental mice were gavaged with the amount of P-80 equal to 1% of their body weight. This amount correlates to the acceptable daily human intake of 1% per kg of polysorbate-80 to body weight [7]. Methods Mice and dietThe C57BL/6 (000664) mice were purchased from The Jackson Laboratory. The mice were maintained under specific pathogenfree conditions, on a 12-h light-dark cycle, and fed normal diet (12 kcal% fat, 29 kcal% protein, 59% kcal carbohydrate) ad libitum. For this study there were two groups: one control group (ingesting saline via gavage) and one experimental P-80 fed group (ingesting P-80 dissolve in saline, 1% per kg via gavage). This dose corresponds to the FDA Acceptable Daily Intake (ADI) in humans (1% per kg (body weight), adjusted to the mouse AbstractThe increasing prevalence of obesity has emerged as one of the most important global public health issue. The change to the human microbiome as a result of changes in the quality and quantity of food intake over the past several decades has been implicated in the development of obesity and metabolic syndrome. We administered polysorbate-80 to mice via gavage. The researchers monitor liver noninvasively using a bioluminescence imaging. For the liver dysfunction we measure the liver enzymes and PAS stain on liver, electron microscopy liver mitochondria. For the assessment of intestinal inflammation we measured fecal LCN2, LPS, MPO and flagellin by ELISA and qPCR. We use confocal microscopy to detect closet bacteria near the epithelium. 16S sequence was used for the composition of microbiota. Compared with control mice, those receiving emulsifier, showed impaired glycemic tolerance, hyperinsulinemia, altered liver enzymes, larger mitochondria and increased gall bladder size. Additionally, mice in the experimental group showed higher levels of DCA, reduced Muc2 RNA expression, reduced m...

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“…Colitogenic bacteria can damage the epithelial barrier functions either directly or via producing toxins. For instance AIEC strain LF82 disrupts the tight junction protein zonula occludens-1 [165] and through binding to the cell adhesion molecule CEACAM 6 can lead to abnormal expression of claudin 2 [166], while enteropathogenic Escherichia coli (EPEC) induces epithelial cell apoptosis by producing a bacterial toxin called cycle inhibiting factor [167]. Both results in an increased intestinal permeability, which permits the penetration of luminal antigens and microbes, that can stimulate pro-inflammatory responses.…”

Section: The Microbiotamentioning

confidence: 99%

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

Gyires¹,

Tóth²,

Zádori

2014

CPD

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Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory condition of the gastrointestinal tract. The two main forms of IBD are Crohn's disease and ulcerative colitis. According to the recent concept the disease is caused by a combination of factors, including genetics, immune dysregulation, barrier dysfunction and the change in microbial flora. Environmental factors, such as changes in diet, antibiotic use, smoking or improved domestic hygiene (e.g. eradication of intestinal helminths) probably contribute to the development and increased prevalence of IBD. Dysregulation of mucosal immunity in IBD causes an overproduction of inflammatory cytokines which resulted in uncontrolled intestinal inflammation. Based on extensive research over the last decade, besides the conventional therapy, there are several novel pathways and specific targets, on which focus new therapeutics. New therapeutics aim 1./ to correct genetic susceptibility by stimulating NOD2 expression, TLR3 signaling or inhibition of TLR4 pathway, 2./ to restore the immune dysregulation by inhibition of pro-inflammatory cytokines (TNF-, IL-6, IL-13, IL-17, IL-18, IL-21), Th1 polarisation (IL-2, IL-12, IL-23, IFN-), T-cell activation, leukocyte adhesion, as well as by immunostimulation (GM-CSF, G-CSF) and anti-inflammatory cytokines (IL-10, IL-11, IFN--1a), 3./ to restore mucosal barrier function and stimulate mucosal healing by different growth factors, such as GH, EGF, KGF, TGF-, VEGF, 4./ to restore the normal bacterial flora by antibiotics, probiotics. However, in spite of these numerous potential targets, the true value and clinical significance of most of the new biologics and molecules are not clear yet.

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Adherent-Invasive Escherichia coli Induce Claudin-2 Expression and Barrier Defect in CEABAC10 Mice and Crohnʼs Disease Patients§

Cited by 84 publications

References 51 publications

Yersinia pseudotuberculosis disrupts intestinal barrier integrity through hematopoietic TLR-2 signaling

Yersinia pseudotuberculosis disrupts intestinal barrier integrity through hematopoietic TLR-2 signaling

Food Additive P-80 Impacts Mouse Gut Microbiota Promoting Intestinal Inflammation, Obesity and Liver Dysfunction

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

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