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A more recent version of this article appeared on November 4, 2005
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Papers In Press, published online ahead of print August 24, 2005
J. Biol. Chem, 10.1074/jbc.M502449200
Submitted on March 4, 2005
Accepted on August 24, 2005

PI 3-kinase is required for rhinovirus-induced airway epithelial cell IL-8 expression

Dawn C. Newcomb, Uma Sajjan, Suparna Nanua, Yue Jia, Adam M. Goldsmith, J. Kelley Bentley, and Marc B. Hershenson

Pediatrics, University of Michigan Medical School, Ann Arbor, MI 48109-0688

Corresponding Author: mhershen{at}umich.edu

Rhinovirus (RV) is a common cause of asthma exacerbations. The signaling mechanisms regulating RV-induced airway epithelial cell responses have not been well-studied. We examined the role of phosphatidylinositol (PI) 3-kinase in RV-induced interleukin (IL)-8 expression. Infection of 16HBE14o- human bronchial epithelial cells with RV39 induced rapid activation of PI 3-kinase and phosphorylation of Akt, a downstream effector of PI 3-kinases. RV39 also colocalized with YFP-Akt-PH, a Citrogen-tagged fluorescent fusion protein encoding the pleckstrin homology domain of Akt, indicating that 3-phosphorylated PI accumulates at the site of RV infection. Inhibition of PI 3-kinase and Akt attenuated RV39-induced nuclear factor (NF)kappa B transactivation and IL-8 expression. Inhibition of PI 3-kinase also blocked internalization of labeled RV39 into 16HBE14o- cells, suggesting that the requirement of PI 3-kinase for RV39-induced IL-8 expression, at least in part, relates to its role in viral endocytosis.


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