Role of Prostaglandins in age related defects in the Immune response against respiratory viral infections
One of the focuses of the Perlman lab is to study immunopathology caused by a respiratory virus, Severe Acute Respiratory Syndrome- Corona virus (SARS-CoV). Increasing defects in the immune system with age have been documented and shown to correlate with worse outcomes after various viral infections such as influenza A, West Nile and severe acute respiratory syndrome (SARS). In the 2002-2003 SARS epidemic more than half of the aged patients (> 65 years) died, while no mortality was observed in patients under 24 years of age.
I am interested in studying the role of prostaglandins in mediating/regulating age related defects in the immune response against respiratory viral infections especially SARS-CoV. Our lab recently reported the age related defects in migration of respiratory DCs to the draining LN, which further resulted in a weak T cell response following respiratory viral infections. This was found to be due to increased levels of PGD2 in the broncheo alveolar lavage fluid in aged mice. Blocking the effect of PGD2 by using a PGD2 receptor antagonist partially reversed these defects. My goal is to examine the source of PGD2 in the lungs of aged mice and also their potential targets.