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Phosphatidylinositol 3-kinase is required for rhinovirus-induced airway epithelial cell interleukin-8 expression.

Abstract
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-kinase. RV39 also colocalized with cit-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 NF-kappaB 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.
AuthorsDawn C Newcomb, Uma Sajjan, Suparna Nanua, Yue Jia, Adam M Goldsmith, J Kelley Bentley, Marc B Hershenson
JournalThe Journal of biological chemistry (J Biol Chem) Vol. 280 Issue 44 Pg. 36952-61 (Nov 04 2005) ISSN: 0021-9258 [Print] United States
PMID16120607 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Interleukin-8
  • NF-kappa B
  • Phosphatidylinositol 3-Kinases
  • Proto-Oncogene Proteins c-akt
Topics
  • Bronchi (cytology, metabolism)
  • Cells, Cultured
  • Electrophoretic Mobility Shift Assay
  • Epithelial Cells (cytology, enzymology)
  • Humans
  • Interleukin-8 (genetics, metabolism)
  • NF-kappa B (metabolism)
  • Phosphatidylinositol 3-Kinases (metabolism)
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins c-akt (metabolism)
  • Respiratory System (cytology, enzymology)
  • Rhinovirus (physiology)
  • Transcription, Genetic

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