| Autor: |
Baiyu Wang, Huifang Guo, Qilong Qiao, Qing Huang, Panpan Yang, Congcong Song, Mingzhen Song, Zeng Wang, Yongtao Li, Yuhe Miao, Jun Zhao |
| Jazyk: |
angličtina |
| Rok vydání: |
2022 |
| Předmět: |
|
| Zdroj: |
Poultry Science, Vol 101, Iss 3, Pp 101695- (2022) |
| Druh dokumentu: |
article |
| ISSN: |
0032-5791 |
| DOI: |
10.1016/j.psj.2021.101695 |
| Popis: |
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. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
|
