MiR-34c and PlncRNA1 mediated the function of intestinal epithelial barrier by regulating tight junction proteins in inflammatory bowel disease

2017 ◽  
Vol 486 (1) ◽  
pp. 6-13 ◽  
Author(s):  
Tanzhou Chen ◽  
Haibo Xue ◽  
Ruoyang Lin ◽  
Zhiming Huang
Keyword(s):  
Inflammatory Bowel Disease ◽  
Tight Junction ◽  
Bowel Disease ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Tight Junction Proteins ◽  
Intestinal Epithelial Barrier ◽  
Inflammatory Bowel ◽  
Junction Proteins

Vitamin A inhibits the action of LPS on the intestinal epithelial barrier function and tight junction proteins

2019 ◽  
Vol 10 (2) ◽  
pp. 1235-1242 ◽  
Author(s):  
Caimei He ◽  
Jun Deng ◽  
Xin Hu ◽  
Sichun Zhou ◽  
Jingtao Wu ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Intestinal Barrier ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Tight Junction Proteins ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Inflammatory Bowel ◽  
Junction Proteins

Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and other diseases.

scholarly journals Tumour Necrosis Factor Superfamily Members in the Pathogenesis of Inflammatory Bowel Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Tomasz J. Ślebioda ◽  
Zbigniew Kmieć
Keyword(s):  
Inflammatory Bowel Disease ◽  
Tumour Necrosis Factor ◽  
Bowel Disease ◽  
Tumour Necrosis ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Inflammatory Conditions ◽  
Inflammatory Bowel ◽  
Necrosis Factor

Inflammatory bowel disease (IBD) is a group of inflammatory conditions of the gastrointestinal tract of unclear aetiology of which two major forms are Crohn’s disease (CD) and ulcerative colitis (UC). CD and UC are immunologically distinct, although they both result from hyperactivation of proinflammatory pathways in intestines and disruption of intestinal epithelial barrier. Members of the tumour necrosis factor superfamily (TNFSF) are molecules of broad spectrum of activity, including direct disruption of intestinal epithelial barrier integrity and costimulation of proinflammatory functions of lymphocytes. Tumour necrosis factor (TNF) has a well-established pathological role in IBD which also serves as a target in IBD treatment. In this review we discuss the role of TNF and other TNFSF members, notably, TL1A, FasL, LIGHT, TRAIL, and TWEAK, in the pathogenesis of IBD.

Dietary fibre-based SCFA mixtures promote both protection and repair of intestinal epithelial barrier function in a Caco-2 cell model

2017 ◽  
Vol 8 (3) ◽  
pp. 1166-1173 ◽  
Author(s):  
Tingting Chen ◽  
Choon Young Kim ◽  
Amandeep Kaur ◽  
Lisa Lamothe ◽  
Maliha Shaikh ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Barrier Function ◽  
Cell Model ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Gut Barrier Function ◽  
Inflammatory Bowel

Impaired gut barrier function plays an important role in the development of many diseases such as obesity, inflammatory bowel disease, and in HIV infection.

scholarly journals Intestinal epithelial barrier function and tight junction proteins with heat and exercise

2016 ◽  
Vol 120 (6) ◽  
pp. 692-701 ◽  
Author(s):  
Karol Dokladny ◽  
Micah N. Zuhl ◽  
Pope L. Moseley
Keyword(s):  
Heat Stress ◽  
Tight Junction ◽  
Barrier Function ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Tight Junction Proteins ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Tight Junction ◽  
Junction Proteins

A single layer of enterocytes and tight junctions (intercellular multiprotein complexes) form the intestinal epithelial barrier that controls transport of molecules through transcellular and paracellular pathways. A dysfunctional or “leaky” intestinal tight junction barrier allows augmented permeation of luminal antigens, endotoxins, and bacteria into the blood stream. Various substances and conditions have been shown to affect the maintenance of the intestinal epithelial tight junction barrier. The primary focus of the present review is to analyze the effects of exertional or nonexertional (passive hyperthermia) heat stress on tight junction barrier function in in vitro and in vivo (animals and humans) models. Our secondary focus is to review changes in tight junction proteins in response to exercise or hyperthermic conditions. Finally, we discuss some pharmacological or nutritional interventions that may affect the cellular mechanisms involved in maintaining homeostasis of the intestinal epithelial tight junction barrier during heat stress or exercise.

scholarly journals P063 HDAC as versatile regulators of the intestinal epithelial barrier in inflammatory bowel disease

2017 ◽  
Vol 11 (suppl_1) ◽  
pp. S109-S109
Author(s):  
M. Friedrich ◽  
J. Ganther ◽  
T. Breiderhoff ◽  
R. Rosenthal ◽  
R. Glauben ◽  
...  
Keyword(s):  
Inflammatory Bowel Disease ◽  
Bowel Disease ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Inflammatory Bowel

scholarly journals Lactobacillus plantarum inhibits intestinal epithelial barrier dysfunction induced by unconjugated bilirubin

2010 ◽  
Vol 104 (3) ◽  
pp. 390-401 ◽  
Author(s):  
Yukun Zhou ◽  
Huanlong Qin ◽  
Ming Zhang ◽  
Tongyi Shen ◽  
Hongqi Chen ◽  
...  
Keyword(s):  
Tight Junction ◽  
Lactobacillus Plantarum ◽  
Laser Scanning Microscopy ◽  
Unconjugated Bilirubin ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Tight Junction Proteins ◽  
Intestinal Epithelial Barrier ◽  
Junction Protein ◽  
Junction Proteins

Although a large number of in vitro and in vivo tests have confirmed that taking probiotics can improve the intestinal barrier, few studies have focused on the relationship between probiotics and the intestinal epithelial barrier in hyperbilirubinaemia. To investigate the effects of and mechanisms associated with probiotic bacteria (Lactobacillus plantarum; LP) and unconjugated bilirubin (UCB) on the intestinal epithelial barrier, we measured the viability, apoptotic ratio and protein kinase C (PKC) activity of Caco-2 cells. We also determined the distribution and expression of tight junction proteins such as occludin, zonula occludens (ZO)-1, claudin-1, claudin-4, junctional adhesion molecule (JAM)-1 and F-actin using confocal laser scanning microscopy, immunohistochemistry, Western blotting and real-time quantitative PCR. The present study demonstrated that high concentrations of UCB caused obvious cytotoxicity and decreased the transepithelial electrical resistance (TER) of the Caco-2 cell monolayer. Low concentrations of UCB inhibited the expression of tight junction proteins and PKC but could induce UDP-glucuronosyltransferases 1 family-polypeptide A1 (UGT1A1) expression. UCB alone caused decreased PKC activity, serine phosphorylated occludin and ZO-1 levels. After treatment with LP, the effects of UCB on TER and apoptosis were mitigated; LP also prevented aberrant expression and rearrangement of tight junction proteins. Moreover, PKC activity and serine phosphorylated tight junction protein levels were partially restored after treatment with LP, LP exerted a protective effect against UCB damage to Caco-2 monolayer cells, and it restored the structure and distribution of tight junction proteins by activating the PKC pathway. In addition, UGT1A1 expression induced by UCB in Caco-2 cells could ameliorate the cytotoxicity of UCB.

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