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Publication : CXCR2 regulates respiratory syncytial virus-induced airway hyperreactivity and mucus overproduction.

First Author  Miller AL Year  2003
Journal  J Immunol Volume  170
Issue  6 Pages  3348-56
PubMed ID  12626595 Mgi Jnum  J:82293
Mgi Id  MGI:2652006 Doi  10.4049/jimmunol.170.6.3348
Citation  Miller AL, et al. (2003) CXCR2 regulates respiratory syncytial virus-induced airway hyperreactivity and mucus overproduction. J Immunol 170(6):3348-56
abstractText  Severe inflammation and mucus overproduction are partially responsible for respiratory syncytial virus (RSV)-induced disease in infants. Using a murine model, we characterized the virally induced chemokine receptors responsible for mediating the pathophysiological response to RSV infection, we found that CXCR2 mRNA was induced at 4 days after RSV infection. Immunohistochemical staining demonstrated that CXCR2 protein was expressed on alveolar macrophages. Immunoneutralization of CXCR2 resulted in decreased airway hyperreactivity relative to the RSV-infected controls. In addition, there was decreased mucus in the bronchoalveolar lavage fluid, decreased periodic-acid Schiff staining, and significantly less mucus-associated gob-5 mRNA and protein in anti-CXCR2-treated mice. The effects of anti-CXCR2 treatment were not a result of differences in viral clearance or neutrophil influx, as these parameters were comparable in both groups of animals. To confirm our immunoneutralization studies, we performed experiments in CXCR2(-/-) mice. Results in CXCR2(-/-) mice recapitulated results from our immunoneutralization studies. However, CXCR2(-/-) mice also showed a statistically significant decrease in muc5ac, relative to RSV-infected wild-type animals. Thus, CXCR2 may be a relevant target in the pathogenesis of RSV bronchiolitis, since it contributes to mucus production and airway hyperreactivity in our model of RSV infection.
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