Abstract
BackgroundInterleukin (IL)-32 is a recently described pro-inflammatory cytokine that has been reported to be induced by bacteria treatment in culture cells. Little is known about IL-32 production by exogenous pathogens infection in human individuals.Methods and FindingsIn this study, we found that IL-32 level was increased by 58.2% in the serum samples from a cohort of 108 patients infected by influenza A virus comparing to that of 115 healthy individuals. Another pro-inflammatory 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 cells was blocked by either selective COX-2 inhibitor NS398 or 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.ConclusionsIL-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.
Highlights
Influenza A virus (IV) is a highly contagious single-stranded RNA virus that infects both the upper and lower respiratory tracts of humans
IL-32 is induced by influenza A virus infection via COX-2 in the inflammatory cascade
Because COX-2 and IL-32 gene expression are associated with inflammatory processes, the aim of this study is to investigate the role of influenza A virus infection in the regulation of IL-32 expression and to determine the molecular mechanisms responsible
Summary
Influenza A virus (IV) is a highly contagious single-stranded RNA virus that infects both the upper and lower respiratory tracts of humans. The host innate immune Toll-like receptor 3 (TLR3) was shown previously in cells of myeloid origin to recognize the viral replicative, intermediate double-stranded RNA (dsRNA). DsRNA is critical for the outcome of the infection and appears to be an active component of viral infection that stimulates antiviral activities. It accumulates during the replication of many viruses [1,2], including influenza virus. TLR3 contributes directly to the immune response of respiratory epithelial cells to influenza A virus and dsRNA [3,4]. Little is known about IL-32 production by exogenous pathogens infection in human individuals
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