Journal
CELLULAR & MOLECULAR IMMUNOLOGY
Volume 12, Issue 5, Pages 633-644Publisher
CHIN SOCIETY IMMUNOLOGY
DOI: 10.1038/cmi.2014.80
Keywords
IL-32; IL-6; inflammation network; influenza A virus; soluble IL-6 receptor
Categories
Funding
- Major State Basic Research Development Program of China [2013CB911102]
- National Natural Science Foundation of China [81271821, 81461130019]
- National Mega Project on Major Infectious Diseases Prevention [2012ZX10004503-004]
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Influenza A virus (IAV) infection is a major worldwide public health problem. However, the factors involved in mediating the inflammatory response to this infection and their relationships remain poorly understood. Here, we show that IAV infection stimulates the expression of the soluble IL-6 receptor (sIL-6R), a multifunctional protein involved in IL-6 signaling. Interestingly, sIL-6R expression upregulated the levels of its own ligand, IL-6 and those of the pro-inflammatory cytokine IL-32. shRNA-mediated knockdown of sIL-6R suppressed IL-6 and IL-32, indicating that this regulation is dependent on sIL-6R during IAV infection. Furthermore, our results demonstrate that IL-32 participates in a negative feedback loop that inhibits sIL-6R while upregulating IL-6 expression during IAV infection. Therefore, we show that sIL-6R is a critical cellular factor involved in the acute inflammatory response to viral infection.
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