›› 2017, Vol. 44 ›› Issue (1): 262-267.doi: 10.16431/j.cnki.1671-7236.2017.01.037

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Molecular Mechanism of the Inflammatory Response Induced by Enterotrxigenic E. coli K88 in Piglets

LI Hai-hua1,2, ZHU Qi1,2, WANG Shi-qiong1,2, YANG Chun-lei1,2, ZHAO Xiang-hua1,2, QIAO Jia-yun1,2, WANG Wen-jie1,2   

  1. 1. Tianjin Institute of Animal Husbandry and Veterinary Science, Tianjin 300381, China;
    2. Tianjin Engineering Research Center for Livestock and Poultry Health Breeding, Tianjin 300381, China
  • Received:2016-06-14 Online:2017-01-20 Published:2017-01-19

Abstract:

To investigate the molecular mechanism of the inflammatory response in the piglets infected with enterotoxigenic E. coli (ETEC) K88, piglets were infected with ETEC K88,the IL-8 content in serum of piglets were assayed by ELISA,and the mRNA relative expression levels of TLR2/4 and its signal transduction pathway related genes (MyD88,Tollip and Bcl3) in mesenteric lymph nodes were detected by quantitative Real-time PCR. The results showed that compared with control group,the content of IL-8 in serum and the expressions of TLR2/4 in lymph nodes were all extremely significantly or significantly increased at 6 and 24 h after infection (P<0.01;P<0.05),and the IL-8 content and TLR2/4 mRNA expression at 24 h after infection were all significantly lower than those at 6 h after infection (P<0.05).In addition,the expressions of MyD88,Tollip and Bcl3 in lymph nodes were all extremely significantly increased at 24 h after infection compared with control group (P<0.01), but there was no significant difference between experimental group and control group at 6 h after infection (P>0.05). In conclusion,ETEC K88 infected piglets might produce inflammatory cytokines IL-8 through the TLR2/4-MyD88 signaling pathway,which could promote the inflammatory reaction in piglets. This inflammatory response might be regulated by Tollip and Bcl3,which could weak the inflammatory intensity in piglets.

Key words: E. coli K88; piglet; inflammatory response; Toll-like receptors; inflammatory regulation

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