Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 287, Issue 15, Pages 11899-11910Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M111.308064
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Funding
- Major State Basic Research Development Program of China (973 project) [2009CB522506, 2012CB518900]
- National Natural Science Foundation of China [30970144, 81171654]
- National Mega Project on Major Infectious Diseases Prevention [2012ZX10004503, 2012ZX10002006-003, 2012ZX10004-207]
- National Mega Project on Major Drug Development [2011ZX09401-302]
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We previously reported that IL-27, which belongs to the IL-12 family of cytokines, is elevated in the serum of patients infected with influenza A virus (IAV). Here, we show that the expression of IL-27 was significantly up-regulated in A549 human lung epithelial cells and human peripheral blood mononuclear cells infected with IAV. Additionally, IAV triggered IL-27 expression through protein kinase A and cAMP-response element-binding protein signaling, which was mediated by cyclooxygenase-2-derived prostaglandin E-2. IL-27 inhibited IAV replication by STAT1/2/3 phosphorylation and activated antiviral factor protein kinase R phosphorylation. Clinical analysis showed that IL-27 levels were significantly elevated in a cohort of patients infected with IAV compared with healthy individuals and that circulating IL-27 levels were tightly and positively correlated with prostaglandin E-2 levels. These results indicate that IL-27 expression is one host immune factor produced in response to IAV infection and that elevated IL-27 levels inhibit viral replication.
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