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

Yu Luo,Bert Devriendt,Eric Cox,Haijian He,Hongbin Zhang,Yanfeng Ma,Chunyan Jiang,Jia Xu,Chaoying Zhang,Yuan Wu

doi:10.1186/s13567-019-0665-8

Yu Luo, Bert Devriendt + Show 8 more

Open Access

https://doi.org/10.1186/s13567-019-0665-8

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Journal: Veterinary Research	Publication Date: Jun 20, 2019
Citations: 12	License type: open-access

Affiliation: Ghent University, Jinhua Polytechnic

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.

Highlights

The importance of the IL-17 cytokine family in inflammation and autoimmunity is well recognized
F4+ enterotoxigenic E. coli (ETEC) induces IL‐17C and TLR2, 5, 8 and ‐10 mRNA expression in small intestinal tissues Previously, we showed that the F 4+ETEC strain GIS26 (O149:K91:F4ac+, LT+STa+STb+) elicited IL-17A mRNA expression in small intestinal tissues [19], so we first determined if another F4+ETEC strain, C83901 (O8:K87:F4ab, LT+, STb+), can induce a similar response
We showed that F4+ ETEC infection triggered IL-17C production in small intestinal epithelial cells in a TLR5-dependent manner

Summary

Introduction

The importance of the IL-17 cytokine family in inflammation and autoimmunity is well recognized. This family consists of six members: IL-17A, IL-17B, IL-17C, IL-17D, IL-17E ( called IL-25) and IL-17F [1]. These cytokines bind to heterodimeric complexes composed of members of the IL-17 family of receptors: IL-17 receptor (IL-17R) A, IL-17RB, IL-17RC, IL-17RD, and IL-17RE, to elicit their biological effects [2]. IL-17A/F initiates innate host defenses and repair responses that include the induction of proinflammatory cytokines and chemokines, antimicrobial peptides and.

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