scholarly journals Protective effects of lactic acid bacteria on gut epithelial barrier dysfunction are Toll like receptor 2 and protein kinase C dependent

2020 ◽  
Vol 11 (2) ◽  
pp. 1230-1234
Author(s):  
Chengcheng Ren ◽  
Qiuxiang Zhang ◽  
Bart J. de Haan ◽  
Marijke M. Faas ◽  
Hao Zhang ◽  
...  
Keyword(s):  
Lactic Acid ◽  
Epithelial Barrier ◽  
Protective Effects ◽  
Toll Like Receptor ◽  
Bacterial Strains ◽  
Barrier Dysfunction ◽  
Barrier Integrity ◽  
Kinase C ◽  
Toll Like Receptor 2 ◽  
Epithelial Barrier Dysfunction

TLR2-signalling lactic acid bacterial strains specifically inhibit PKC-dependent gut epithelial barrier integrity loss but cannot dampen MAPK-dependent epithelial barrier disruption.

scholarly journals The Protective Effects of a Synthetic Geranyl Acetophenone in a Cellular Model of TNF-α-Induced Pulmonary Epithelial Barrier Dysfunction

Molecules ◽  
2018 ◽  
Vol 23 (6) ◽  
pp. 1355 ◽  
Author(s):  
Tee Sim ◽  
Hanis Harith ◽  
Chau Tham ◽  
Nur Md Hashim ◽  
Khozirah Shaari ◽  
...  
Keyword(s):  
Epithelial Barrier ◽  
Protective Effects ◽  
Cellular Model ◽  
Barrier Dysfunction ◽  
Tnf Α ◽  
Epithelial Barrier Dysfunction

Tu1376 Protective Effects of Partially Hydrolyzed Guar Gum Against Intestinal Epithelial Barrier Dysfunction

2015 ◽  
Vol 148 (4) ◽  
pp. S-874
Author(s):  
Atsushi Majima ◽  
Yuji Naito ◽  
Osamu Handa ◽  
Yuriko Onozawa ◽  
Yukiko Uehara ◽  
...  
Keyword(s):  
Guar Gum ◽  
Epithelial Barrier ◽  
Protective Effects ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Dysfunction ◽  
Partially Hydrolyzed Guar Gum

scholarly journals Toll-like receptor 2 stimulation augments esophageal epithelial barrier integrity

2019 ◽  
Author(s):  
Melanie A. Ruffner ◽  
Li Song ◽  
Kelly Maurer ◽  
Lihua Shi ◽  
Margaret C. Carroll ◽  
...  
Keyword(s):  
Tight Junction ◽  
Chromatin Immunoprecipitation ◽  
Three Dimensional ◽  
Receptor Expression ◽  
Epithelial Barrier ◽  
Toll Like Receptor ◽  
Barrier Integrity ◽  
Tight Junction Complex ◽  
Toll Like Receptor 2

AbstractBackgroundA key concept of the hygiene hypothesis is that the microbiome modulates both epithelial barrier integrity as well as host immune responses. Defective expression of tight junction complex proteins alters this homeostatic process, and plays a role in atopic disorders including eosinophilic esophagitis. We tested the hypothesis that Toll-like receptor 2 (TLR2) stimulation improves esophageal barrier function in a cell-intrinsic manner by upregulation of TJ-protein expression using an in vitro model of human epithelium.MethodsPattern recognition receptor expression was assessed in esophageal epithelial cells from patients with EoE and non-EoE control patients. Functional consequences of TLR2 stimulation were investigated using human esophageal EPC2-hTERT cells in the three-dimensional air-liquid interface culture (ALI) model to evaluate transepithelial electrical resistance (TEER) and FITC-Dextran permeability. Characterization of TLR2-stimulated ALI cultures was performed by histology, immunohistochemistry, western blotting and chromatin immunoprecipitation.ResultsTLR2 stimulation increased TEER (1.28 to 1.31-fold) and decreased paracellular permeability to FITC-Dextran. Notably, TLR2 stimulation-induced increases in TEER were abolished by treatment with anti-TLR2 blocking antibody. Tight junction complex proteins claudin 1 and zonula occludens 1 were increased following TLR2 stimulation, and chromatin immunoprecipitation analysis demonstrated significant increase in histone 4 acetyl binding at the CLDN1 enhancer and promoter following zymosan treatment, implying the occurrence of durable chromatin changes in the esophageal epithelium.ConclusionsOur findings reveal that the TLR2 pathway may play a regulatory role as a mechanism that maintains epithelial barrier homeostasis in the esophagus.

scholarly journals Curcumin Mitigates Immune-Induced Epithelial Barrier Dysfunction by Campylobacter jejuni

2019 ◽  
Vol 20 (19) ◽  
pp. 4830 ◽  
Author(s):  
Fábia Daniela Lobo de Sá ◽  
Eduard Butkevych ◽  
Praveen Kumar Nattramilarasu ◽  
Anja Fromm ◽  
Soraya Mousavi ◽  
...  
Keyword(s):  
Campylobacter Jejuni ◽  
Curcuma Longa ◽  
Epithelial Barrier ◽  
Protective Agent ◽  
Protective Effects ◽  
Barrier Dysfunction ◽  
Natural Polyphenol ◽  
Electrophysiological Measurements ◽  
Medical Plant ◽  
Epithelial Barrier Dysfunction

Campylobacter jejuni (C. jejuni) is the most common cause of foodborne gastroenteritis worldwide. The bacteria induce diarrhea and inflammation by invading the intestinal epithelium. Curcumin is a natural polyphenol from turmeric rhizome of Curcuma longa, a medical plant, and is commonly used in curry powder. The aim of this study was the investigation of the protective effects of curcumin against immune-induced epithelial barrier dysfunction in C. jejuni infection. The indirect C. jejuni-induced barrier defects and its protection by curcumin were analyzed in co-cultures with HT-29/B6-GR/MR epithelial cells together with differentiated THP-1 immune cells. Electrophysiological measurements revealed a reduction in transepithelial electrical resistance (TER) in infected co-cultures. An increase in fluorescein (332 Da) permeability in co-cultures as well as in the germ-free IL-10−/− mouse model after C. jejuni infection was shown. Curcumin treatment attenuated the C. jejuni-induced increase in fluorescein permeability in both models. Moreover, apoptosis induction, tight junction redistribution, and an increased inflammatory response—represented by TNF-α, IL-1β, and IL-6 secretion—was observed in co-cultures after infection and reversed by curcumin. In conclusion, curcumin protects against indirect C. jejuni-triggered immune-induced barrier defects and might be a therapeutic and protective agent in patients.

scholarly journals Salmonella Effector SpvB Disrupts Intestinal Epithelial Barrier Integrity for Bacterial Translocation

2020 ◽  
Vol 10 ◽  
Author(s):  
Lanqing Sun ◽  
Sidi Yang ◽  
Qifeng Deng ◽  
Kedi Dong ◽  
Yuanyuan Li ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Junctional Complex ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Intestinal Epithelial Barrier ◽  
Barrier Integrity ◽  
Epithelial Barrier Dysfunction

Salmonella are common enteric bacterial pathogens that infect both humans and animals. Intestinal epithelial barrier, formed by a single layer of epithelial cells and apical junctional complex (AJC), plays a crucial role in host defense against enteric pathogens to prevent bacterial translocation. However, the underlying mechanisms of intestinal epithelial barrier dysfunction caused by Salmonella are poorly understood. It is found that a locus termed Salmonella plasmid virulence (spv) gene exists extensively in clinically important Salmonella serovars. SpvB is a key effector encoded within this locus, and closely related to Salmonella pathogenicity such as interfering with autophagy and iron homeostasis. To investigate the interaction between SpvB and intestinal epithelial barrier and elucidate the underlying molecular mechanism, we used the typical foodborne disease agent Salmonella enterica serovar Typhimurium (Salmonella typhimurium) carrying spvB or not to construct infection models in vivo and in vitro. C57BL/6 mice were orally challenged with S. typhimurium wild-type strain SL1344 or spvB-deficient mutant strain SL1344-ΔspvB. Caco-2 cell monolayer model, as a widely used model to mimic the human intestinal epithelium in vitro, was infected with SL1344, SL1344-ΔspvB, or spvB complementary strain SL1344-c-ΔspvB, respectively. The results showed that SpvB enhanced bacterial pathogenicity during S. typhimurium infection in vivo, and contributed to intestinal epithelial barrier dysfunction in both infection systems. This SpvB-mediated barrier dysfunction was attributed to the cellular redistribution of Claudin-1, Occludin, and E-cadherin junctional proteins. Moreover, by using pharmacological inhibitors, we found that F-actin rearrangement and suppression of protein kinase C (PKC) signaling pathway were involved in SpvB-mediated barrier dysfunction. In conclusion, the study reveals the contribution of Salmonella effector SpvB to the dysfunction of intestinal epithelial barrier integrity, which facilitates bacterial translocation via the paracellular route to promote Salmonella systemic dissemination. Our findings broaden the understanding of host–pathogen interactions in salmonellosis, and provide new strategies for the therapy in limiting bacterial dissemination during infection.

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