Hypervirulent FAdV-4 infection induces activation of the NLRP3 inflammasome in chicken macrophages

Poultry Science

Baiyu Wang¹  Qing Huang¹  Qilong Qiao¹  Huifang Guo¹  Yongtao Li¹  Jun Zhao¹  Mingzhen Song¹  Zeng Wang¹  Congcong Song¹  Panpan Yang²  Yuhe Miao² 

[1] College of Veterinary Medicine, Henan Agricultural University, Zhengzhou 450046, China;Fujian Shengwei Biotech Co., Ltd., Nanping 354100, China;

关键词: fowl adenovirus serotype 4;    NLRP3 inflammasome;    Caspase-1;    interleukin-1 beta;    chicken macrophage;   

DOI  :  

来源: DOAJ

【 摘 要 】

ABSTRACT: Fowl adenovirus serotype 4 (FAdV-4) is the primary causative agent of hepatitis–hydropericardium syndrome (HHS) causing great economic losses to the world poultry industry. The exact factors responsible for the pathogenesis of hypervirulent FAdV-4 have not been completely elucidated. Hypervirulent FAdV-4 infection induces inflammatory damages in accompany with a high level of proinflammatory interleukin-1 beta (IL-1β) secretion in a variety of organs. Investigation of the mechanisms underlying hypervirulent FAdV-4-induced IL-1β secretion would contribute to understanding of the pathogenesis of FAdV-4. Here, we investigated whether FAdV-4 infection activates NLRP3 inflammasome in chicken macrophage cell line HD11. The results showed that stimulation of HD11 with hypervirulent FAdV-4 induced NLRP3- and Caspase-1-dependent secretion of IL-1β. Genetic knockdown of NLRP3 or Caspase-1 expression, a critical component of inflammasome, significantly downregulated IL-1β expression, indicating that activation of the NLRP3 inflammasome contributed to the FAdV-4-induced IL-1β secretion. Moreover, ATP signaling and potassium efflux were involved in the process of NLRP3 inflammasome activation. Our data indicated that hypervirulent FAdV-4 infection induces the activation of NLRP3 inflammasome and followed by massive secretion of IL-1β of macrophages, which thereby contribute to the inflamed lesion of tissues.

【 授权许可】

Unknown