Journal
MICROBES AND INFECTION
Volume 8, Issue 14-15, Pages 2880-2889Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.micinf.2006.09.007
Keywords
virus; IL-13; interferon
Categories
Funding
- NHLBI NIH HHS [R01-HL-069949, R01 HL069449, R01 HL069949] Funding Source: Medline
- NIAID NIH HHS [R01 AI045512, R01-AI-045512, R01-AI-054660, R01 AI054660] Funding Source: Medline
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The role of IL-13 in respiratory syncytial virus (RSV) immunopathogenesis is incompletely described. To assess the effect of IL-13 on primary RSV infection, transgenic mice which either overexpress IL-13 in the lung (IL-13 OE) or non-transgenic littermates (IL-13 NT) were challenged intranasally with RSV. IL-13 OE mice had significantly decreased peak viral titers four days after infection compared to non-transgenic littermates. In addition, IL-13 OE mice had significantly lower RSV-induced weight loss and reduced lung IFN-gamma protein expression compared with IL-13 NT mice. In contrast, primary RSV challenge of IL-13 deficient mice resulted in a small, but statistically significant increase in viral titers on day four after infection, no difference in RSV-induced weight loss compared to wild type mice, and augmented IFN-gamma production on day 6 after infection. In STAT1-deficient (STAT1 KO) mice, where primary RSV challenge produced high levels of IL-13 production in the lungs, treatment with an IL-13 neutralizing protein resulted in greater peak viral titers both four and six days after RSV and greater RSV-induced weight loss compared to mice treated with a control protein. These results suggest that IL-13 modulates illness from RSV-infection. (c) 2006 Elsevier Masson SAS. All rights reserved.
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