Beta-chemokines in nasal secretions of infants with respiratory syncytial virus-induced respiratory infections

Immune mechanisms are believed to contribute to the pathogenesis of bronchiolitis, but the nature of the critical pathways is unknown. The purpose of this study was to determine if quantities of the beta-chemokines macrophage inflammatory protein 1 alpha (MIP1α), eotaxin, and regulated on expression, normal T-cell expressed and secreted (RANTES) were different among infants with various forms of illness due to respiratory syncytial virus (RSV) infection. Samples of nasopharyngeal secretions (NPS) were obtained from 56 infants and children less than 13 months of age with either upper respiratory illness (URI) alone (n = 25) or lower respiratory tract illness (n = 31) due to RSV infection. Seventeen asymptomatic infants served as controls. Quantities of chemokines in secretions were compared between groups using the t-test after logarithmic transformation of data. Quantities of all three chemokines were increased at the time of RSV infection regardless of whether wheezing was present. However, concentrations of MIP-1α were significantly greater (p = 0.039) in wheezing infants than in those with URI alone. Quantities of MIP-1α (p = 0.029) and eotaxin (p = 0.017) were each significantly greater in wheezing infants with hypoxia than wheezing infants without hypoxia, and were inversely related to individual values of oxygen saturation. Finally, all three chemokines were still present at high levels in secretions for at least 2 to 3 weeks after respiratory symptoms had improved. These findings permit the hypothesis that MIP-1α may possibly play a role in the induction of inflammation and wheezing at the time of RSV infection.