CD8 T cells are essential in the development of respiratory syncytial virus-induced lung eosinophilia and airway hyperresponsiveness

Viral respiratory infections can cause bronchial hyperresponsiveness and ex acerbate asthma, In mice, respiratory syncytial virus (RSV) infection resul ts in airway hyperresponsiveness (AHR) and eosinophil influx into the airwa ys. The immune cell requirements for these responses to RSV infection are n ot well defined. To delineate the role of CD8 T cells in the development of RSV-induced AHR and lung eosinophilia, we tested the ability of mice deple ted of CDS T cells to develop these symptoms of RSV infection. BALB/c mice were depleted of CD8 T cells using anti-CD8 Ab treatment before intranasal administration of infectious RSV, Six days postinfection, airway responsive ness to inhaled methacholine was assessed by barometric body plethysmograph y, and numbers of lung eosinophils and levels of IFN-gamma, IL-4, and IL-5 in bronchoalveolar lavage fluid were monitored. RSV infection resulted in a irway eosinophilia and AHR in control mice, but not in CDS-depleted animals . Further, whereas RSV-infected mice secreted increased amounts of IL-5 int o the airways as compared with noninfected controls, no IL-5 was detectable in both bronchoalveolar lavage fluid and culture supernatants from CDS-dep leted animals. Treatment of CDS-depleted mice with IL-5 fully restored both lung eosinophilia and AHR. We conclude that CD8 T cells are essential for the influx of eosinophils into the lung and the development of AHR in respo nse to RSV infection.