title: Transfer of the enhancing effect of respiratory syncytial virus infection on subsequent allergic airway sensitization by T lymphocytes.
abstract: In mice, respiratory syncytial virus (RSV) infection enhances allergic airway sensitization, resulting in lung eosinophilia and in airway hyperresponsiveness (AHR). The mechanisms by which RSV contributes to development of asthma and its effects on allergic airway sensitization in mice are not known. We tested whether these consequences of RSV infection can be adoptively transferred by T cells and whether depletion of T cell subsets prevents the effects of RSV infection on subsequent airway sensitization. Mononuclear cells, T lymphocytes, or CD4 or CD8 T cells from peribronchial lymph nodes (PBLN) of RSV-infected mice were transferred into naive BALB/c mice which were then exposed to OVA via the airways. Additionally, RSV-infected mice were depleted of CD4 or CD8 T cells following acute RSV infection but prior to airway sensitization. Following sensitization, airway responsiveness to inhaled methacholine, numbers of lung eosinophils, and levels of IFN-gamma, IL-4, and IL-5 in PBLN cell cultures were monitored. Transfer of T cells from RSV-infected mice resulted in increased eosinophil influx into the lungs, increased IL-5 production, and development of AHR following airway sensitization to allergen. Transfer of CD8 but not CD4 T cells from the PBLN of RSV-infected mice also resulted in AHR following 10 days of OVA exposure. Further, depletion of CD8 T cells prevented these consequences of RSV infection while CD4 T cell depletion reduced them. We conclude that T cells, in particular CD8 T cells, are critical in mediating RSV-induced development of lung eosinophilia and AHR following allergic airway sensitization.
authors.affiliation: Division of Basic Sciences, Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206, USA.
authors.forename: J
authors.initials: J
authors.lastname: Schwarze
authors.forename: M
authors.initials: M
authors.lastname: Mäkelä
authors.forename: G
authors.initials: G
authors.lastname: Cieslewicz
authors.forename: A
authors.initials: A
authors.lastname: Dakhama
authors.forename: M
authors.initials: M
authors.lastname: Lahn
authors.forename: T
authors.initials: T
authors.lastname: Ikemura
authors.forename: A
authors.initials: A
authors.lastname: Joetham
authors.forename: E W
authors.initials: EW
authors.lastname: Gelfand
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D001980:Bronchi / Q000166:cytology / Q000637:transplantation; D016535:Bronchial Hyperreactivity / Q000276:immunology / Q000517:prevention & control; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002465:Cell Movement / Q000276:immunology; D004802:Eosinophilia / Q000276:immunology / Q000517:prevention & control; D004804:Eosinophils / Q000276:immunology / Q000473:pathology; D005260:Female; D007963:Leukocytes, Mononuclear / Q000637:transplantation; D008168:Lung / Q000276:immunology / Q000473:pathology; D008198:Lymph Nodes / Q000166:cytology / Q000637:transplantation; D008212:Lymphocyte Depletion; D051379:Mice; D008807:Mice, Inbred BALB C; D012130:Respiratory Hypersensitivity / Q000276:immunology*; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D016176:T-Lymphocyte Subsets / Q000637:transplantation* / Q000821:virology*