Journal
FEBS LETTERS
Volume 587, Issue 18, Pages 3014-3020Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2013.07.025
Keywords
Interferon response factor-3; Poly I:C; ERK MAP-kinase; Interleukin-6; Macrophages; Nitric oxide
Funding
- University of Nebraska Medical Center College of Dentistry
- University of Nebraska Lincoln, School of Biological Sciences
- National Institute of General Medicine, a component of the National Institutes of Health (NIH) [P30GM10350903, P20GM103489]
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Understanding nitric oxide (NO) in innate anti-viral immunity and immune-mediated pathology is hampered by incomplete details of its transcriptional and signaling factors. We found in macrophages that IRF3, ERK MAP-kinases, and PKR are essential to NO production in response to RNA-virus mimic, poly I: C, a TLR3 agonist. ERK's role in NO induction may be through phosphorylation of serine-171 of IRF3 and expression of NO-inducing cytokines, IL-6 and IFN-beta. However, these cytokines induced less NO in IRF3 knockout or knockdown macrophages. These findings show that ERK and IRF3 coordinate induction of NO by macrophages in response to stimulation of TLR3. (C) 2013 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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