title: 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 induced by bacteria treatment in culture cells. Little is known about IL-32 production by exogenous pathogens infection in human individuals.
  
  
  RESULTS
  In 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 PGE(2) 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.
authors.affiliation: State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, People's Republic of China.
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Yan
authors.initials: Y
authors.lastname: Liu
authors.forename: Muhammad Mahmood
authors.initials: MM
authors.lastname: Mukhtar
authors.forename: Rui
authors.initials: R
authors.lastname: Gong
authors.forename: Ying
authors.initials: Y
authors.lastname: Pan
authors.forename: Sahibzada T
authors.initials: ST
authors.lastname: Rasool
authors.forename: Yecheng
authors.initials: Y
authors.lastname: Gao
authors.forename: Lei
authors.initials: L
authors.lastname: Kang
authors.forename: Qian
authors.initials: Q
authors.lastname: Hao
authors.forename: Guiqing
authors.initials: G
authors.lastname: Peng
authors.forename: Yanni
authors.initials: Y
authors.lastname: Chen
authors.forename: Xin
authors.initials: X
authors.lastname: Chen
authors.forename: Jianguo
authors.initials: J
authors.lastname: Wu
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhu
mesh_terms: D000328:Adult; D001241:Aspirin / Q000494:pharmacology; D045744:Cell Line, Tumor; D016207:Cytokines / Q000378:metabolism; D005260:Female; D006801:Humans; D007249:Inflammation; D009980:Influenza A virus / Q000378:metabolism*; D007378:Interleukins / Q000378:metabolism*; D019746:Intramolecular Oxidoreductases / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009578:Nitrobenzenes / Q000494:pharmacology; D000071876:Prostaglandin-E Synthases; D034741:RNA, Small Interfering / Q000378:metabolism; D013449:Sulfonamides / Q000494:pharmacology; D014162:Transfection
chemical_list: D016207:Cytokines; C496971:IL32 protein, human; D007378:Interleukins; D009578:Nitrobenzenes; D034741:RNA, Small Interfering; D013449:Sulfonamides; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D019746:Intramolecular Oxidoreductases; D000071876:Prostaglandin-E Synthases; D001241:Aspirin