Respiratory syncytial virus infection activates STAT signaling in human epithelial cells |
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Authors: | Kong Xiaoyuan San Juan Homero Kumar Mukesh Behera Aruna K Mohapatra Alexander Hellermann Gary R Mane Srikant Lockey Richard F Mohapatra Shyam S |
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Institution: | Division of Allergy and Immunology, The Joy McCann Culverhouse Airway Disease Center, Department of Internal Medicine, University of South Florida College of Medicine, Tampa, FL 33612, USA. |
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Abstract: | Acute respiratory syncytial virus (RSV) infection causes airway inflammation and exacerbates asthma, but the mechanism of inflammation is poorly understood. The role of the STAT-signaling pathway in RSV infection in epithelial cells was examined in this study. DNA microarray analyses of RSV-infected human alveolar type II (A549) epithelial cells identified several genes whose expression was altered from -5.5 to +56.4-fold. Four of the highly expressed genes contained STAT-binding elements. In A549 and normal human bronchial epithelial cells (NHBE), RSV induced phosphorylation and nuclear translocation of STAT-1alpha that was abrogated when RSV attachment was blocked. Treatment with a JAK-2 inhibitor or transfection with dominant-negative STAT-1alpha blocked STAT-1alpha activation and RSV infection. RSV also activated STAT-3 and IL-6 specific antibodies blocked this activation. Thus, activation of the STAT-1alpha and STAT-3 pathways play a role in RSV infection. |
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