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PLoS One. 2008 Apr 16;3(4):e1985. doi: 10.1371/journal.pone.0001985.

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

Author information

1
State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, People's Republic of China.

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.

METHODS AND FINDINGS:

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.

PMID:
18414668
PMCID:
PMC2288676
DOI:
10.1371/journal.pone.0001985
[Indexed for MEDLINE]
Free PMC Article

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