Porcine reproductive and respiratory syndrome virus activates inflammasomes of porcine alveolar macrophages via its small envelope protein E

• We proved PRRSV could activate inflammasome in porcine macrophages.
• Inflammasome activation induced by PRRSV was related to its envelope protein E.
• Inflammasome activation might be the cause of PRRSV-induced infected tissue damage.
• This research may provide a potential therapeutic target for PRRS control.

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-1β maturation/release and subsequently induce tissue inflammation and injury. Our results showed that PRRSV and its small envelope protein E significantly increased IL-1β release from LPS-primed PAMs; however, only PRRSV not protein E significantly increased IL-1β 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.