Respiratory syncytial virus infection activates STAT signaling in human epithelial cells

X Kong, H San Juan, M Kumar, AK Behera… - Biochemical and …, 2003 - Elsevier
X Kong, H San Juan, M Kumar, AK Behera, A Mohapatra, GR Hellermann, S Mane…
Biochemical and Biophysical Research Communications, 2003Elsevier
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 …
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-1α that was abrogated when RSV attachment was blocked. Treatment with a JAK-2 inhibitor or transfection with dominant-negative STAT-1α blocked STAT-1α activation and RSV infection. RSV also activated STAT-3 and IL-6 specific antibodies blocked this activation. Thus, activation of the STAT-1α and STAT-3 pathways play a role in RSV infection.
Elsevier