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Toll 样受体 5 介导的肠上皮细胞中白介素-17C 的表达增强了上皮细胞对 F4 型肠产毒性大肠杆菌感染的宿主防御。

Toll-like receptor 5-mediated IL-17C expression in intestinal epithelial cells enhances epithelial host defense against F4 ETEC infection.

机构信息

Animal Medical Testing Center, Department of Animal Production, Faculty of Agricultural & Biological Engineering, Jinhua Polytechnic, Jinhua, China.

Laboratory of Immunology, Faculty of Veterinary Medicine, Ghent University, Ghent, Belgium.

出版信息

Vet Res. 2019 Jun 20;50(1):48. doi: 10.1186/s13567-019-0665-8.

Abstract

Enterotoxigenic Escherichia coli (ETEC) are an important cause of post-weaning diarrhea (PWD) in piglets. The IL-17 cytokine family is well known to play important roles in the host defense against bacterial infections at the mucosa. Previously, we reported the potential role of IL-17A in clearing an ETEC infection in piglets. IL-17C, another member of the IL-17 family, is highly expressed in the intestinal epithelium, however, its role during an ETEC infection is still unclear. In this study, we demonstrate that F4 ETEC induce IL-17C mRNA and protein expression in intestinal tissues as well as in porcine intestinal epithelial cells (IPEC-J2). This IL-17C production is largely dependent on TLR5 signaling in IPEC-J2 cells. Both F4 ETEC infection and exogenous IL-17C increased the expression of antimicrobial peptides and tight junction proteins, such as porcine beta-defensin (pBD)-2, claudin-1, claudin-2 and occludin in IPEC-J2 cells. Taken together, our data demonstrate that TLR5-mediated IL-17C expression in intestinal epithelial cells enhances mucosal host defense responses in a unique autocrine/paracrine manner in the intestinal epithelium against ETEC infection.

摘要

肠产毒性大肠杆菌(ETEC)是仔猪断奶后腹泻(PWD)的重要病因。IL-17 细胞因子家族在宿主抵御粘膜细菌感染方面起着重要作用。先前,我们报道了 IL-17A 在清除仔猪 ETEC 感染中的潜在作用。IL-17C 是 IL-17 家族的另一个成员,在肠上皮细胞中高度表达,但其在 ETEC 感染中的作用尚不清楚。在这项研究中,我们证明 F4 ETEC 诱导肠组织和猪肠上皮细胞(IPEC-J2)中 IL-17C mRNA 和蛋白表达。这种 IL-17C 的产生在很大程度上依赖于 IPEC-J2 细胞中的 TLR5 信号。F4 ETEC 感染和外源性 IL-17C 均增加了抗菌肽和紧密连接蛋白的表达,如猪β防御素(pBD)-2、Claudin-1、Claudin-2 和 Occludin 在 IPEC-J2 细胞中。总之,我们的数据表明,TLR5 介导的肠上皮细胞中 IL-17C 的表达以独特的自分泌/旁分泌方式增强了肠上皮细胞对 ETEC 感染的粘膜宿主防御反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f92e/6584996/3366a70f0ed2/13567_2019_665_Fig1_HTML.jpg

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