Respiratory syncytial virus (RSV) suppression of glucocorticoid receptor phosphorylation does not account for repression of transactivation.
Respiratory syncytial virus (RSV)-induced bronchiolitis in infants, although inflammatory in nature, is not responsive to glucocorticoids. We have recently shown that RSV-infected lung epithelial cells have impaired glucocorticoid receptor (GR)-mediated transactivation. In this study, we show that the N-terminal region of GR is required for RSV repression of GR transactivation and that RSV infection of lung epithelial cells reduces ligand-dependent GR phosphorylation at serine 211 and serine 226. However, we also show that these changes in GR phosphorylation do not account for the RSV repression of GR transactivation suggesting other regions of the GR N-terminus must also be involved.
Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Department of Internal Medicine, Wexner Medical Center at The Ohio State University, Columbus, OH 43210, United States ; Institute for Behavioral Medicine Research, Wexner Medical Center at The Ohio State University, Columbus, OH 43210, United States.
Jeanette I
JI
Webster Marketon
Jacqueline
J
Corry
Glucocorticoid receptor; Phosphorylation; Protein phosphatase; Respiratory syncytial virus; Transactivation