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

• Published in: PloS one 2008-04, Vol.3 (4), p.e1985-e1985
• Main Authors: Li, Wei, Liu, Yan, Mukhtar, Muhammad Mahmood, Gong, Rui, Pan, Ying, Rasool, Sahibzada T, Gao, Yecheng, Kang, Lei, Hao, Qian, Peng, Guiqing, Chen, Yanni, Chen, Xin, Wu, Jianguo, Zhu, Ying
• Format: Article
• Language: English
• Subjects: Acids; Adult; Antigens; Arthritis; Aspirin; Aspirin - pharmacology; Bacteria; Biosynthesis; Cell culture; Cell Line, Tumor; Colorectal cancer; COX-2 inhibitors; Cyclooxygenase-2; Cytokines; Cytokines - metabolism; Drugs; Enzymes; Epithelial cells; Female; Gene expression; Health aspects; Hepatitis; Humans; Immunology/Immunity to Infections; Infections; Infectious Diseases/Respiratory Infections; Inflammation; Influenza; Influenza A; Influenza A virus - metabolism; Influenza viruses; Interleukins; Interleukins - metabolism; Intramolecular Oxidoreductases - metabolism; Laboratories; Life sciences; Lungs; Male; Medical research; Middle Aged; Nitrobenzenes - pharmacology; Overexpression; Prostaglandin E2; Prostaglandin-E Synthases; Prostaglandins E; RNA, Small Interfering - metabolism; Rodents; siRNA; Studies; Sulfonamides - pharmacology; Transfection; Tumor necrosis factor-TNF; Viral infections; Virology; Virology/Effects of Virus Infection on Host Gene Expression; Viruses
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0001985

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. 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. 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.