期刊
VIROLOGY
卷 442, 期 2, 页码 156-162出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2013.04.007
关键词
Porcine reproductive and respiratory; syndrome virus; Envelope protein E; Inflammasomes; Macrophages; Interleukin-1 beta
类别
资金
- National Natural Science Foundation of China [31140093]
- State Key Research Program [2009ZX08006-O1OB]
- Natural Science Foundation of Hebei Province [C2008000244]
Porcine reproductive and respiratory syndrome virus (PRRSV) infection results in extensive tissue inflammation and damage, which are believed to be responsible for increased susceptibility to secondary infection and even for death. However, its pathogenic mechanisms are not fully understood. To explore the mechanism underlying the PRRSV-induced tissue inflammation and damage, we investigated whether PRRSV activates porcine alveolar macrophage (PAM) inflammasomes which mediate por-IL-1 beta maturation/release and subsequently induce tissue inflammation and injury. Our results showed that PRRSV and its small envelope protein E significantly increased IL-1 beta release from LPS-primed PAMs; however, only PRRSV not protein E significantly increased IL-1 beta release from no-LPS-primed PAMs, which indicates PRRSV can activate inflammasomes of PAMs by its encoded protein E. These results provide a molecular basis for the pathogenic mechanism of PRRSV on inducing extensive tissue inflammation and damage, and suggest that the inflammasome may provide a potential therapeutic target for PRRS prevention and treatment. (C) 2013 Elsevier Inc. All rights reserved.
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