Sustained increases in numbers of pulmonary dendritic cells after respiratory syncytial virus infection.

Abstract

Respiratory syncytial virus (RSV) bronchiolitis in infants can lead to wheezing and early allergic sensitization. In mice, RSV infection enhances allergic airway inflammation and airway hyperresponsiveness. Dendritic cells are critical in inducing T-cell responses to both viruses and allergens and could be pivotal in regulating interactions between these. This study addresses the effects of RSV infection on phenotype and function of pulmonary dendritic cells. BALB/c mice were infected with RSV, and expression of CD11c, MHC II, and CD86 on lung and spleen cells was monitored by flow cytometry for 21 days after infection. CD11c(+) cells were isolated to assess their phagocytic capacity and their ability to induce proliferation in allogenic T cells. Numbers of pulmonary CD11c(+) MHC II(hi) cells increased 13-fold starting from day 6 after RSV infection. This was associated with increased CD86 expression, reduced phagocytosis, and increased allogenic T-cell stimulatory capacity in CD11c(+) cells. These changes in the lung outlasted acute infection and were not observed in spleens. RSV infection results in sustained increases in numbers of mature dendritic cells in the lung. These might well contribute to the development of intense airway inflammation and airway hyperresponsiveness after RSV infection and to enhancement of subsequent responses to allergen exposure.