Activation of interleukin-32 pro-inflammatory pathway in response to influenza A virus infection

Abstract

Background: Interleukin (IL)-32 is a recently described pro-inflammatory cytokine that has been reported to be incluced by bacteria treatment in culture cells. Little is know about IL-32 production by exogenous pathogens infection in human individuals. Methods and Findings: In this study, we found that IL-32 tevel was increased by 58.2% in the serum samples from a cohort of 108 patiens infected by influenza A virus comparing to that of 115 healthy individuals. Another pro-unflammatory factor cyclooxygenase (COX)-2-associated prostaglandin E2 was also upregulated by 2.7-fold. Expression of IL-32 in influenza A virus infected A549 human lung epithelial cell was bloked by either selective COX-2 inhibitor NS398 os Aspirin, a known anti-inflammatory drug, indicating IL-32 was induced through COX-2 in the inflammatory cascade. Interestingly, we found that COX-2-associate PGE2 production activated by influenza virus infection was significantly suppressed by over-expression of IL-32 but increased by IL-32-specific sIRNA suggesting there was a feedback mechanism between IL-32 and COX-2. Conclusions: IL-32 is induced by influenza A virus infection via COX-2 in the inflammatory cascade. Our results provide that IL-32 is a potential target for anti-inflammatory medicine screening. © 2008 Li et al.