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Toll-like receptor 5-mediated IL-17C expression in intestinal epithelial cells enhances epithelial host defense against F4+ ETEC infection
- Luo, Yu, Xu, Jia, Zhang, Chaoying, Jiang, Chunyan, Ma, Yanfeng, He, Haijian, Wu, Yuan, Devriendt, Bert, Cox, Eric, Zhang, Hongbin
- Veterinary research 2019 v.50 no.1 pp. 48
- Toll-like receptor 5, antimicrobial peptides, autocrine signaling, bacterial infections, diarrhea, enterotoxigenic Escherichia coli, interleukin-17, intestinal mucosa, messenger RNA, occludins, piglets, protein synthesis, tight junctions
- 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.