Intranasal exposure to the iNKT cell ligand α-galactosylceramide (α-GC) with RSV primary infection in neonatal mice elicited neither cytokine production (except for a slight increase of IL-5) nor pulmonary eosinophilia, despite the presence of both CD1d+ cells and NKT cells.
These findings suggest that a subgroup of the RSV-induced bronchiolitis group results in a T(H)2-type response, and this could provide a valuable framework to explain the link between RSV-induced bronchiolitis and asthma.
To investigate the genetic basis for RSV disease severity, linked variants of 3 Th2 cytokine genes, IL4, IL13, and IL5 (which are clustered on chromosome 5q31.1) were characterized in 105 children who were hospitalized with severe RSV infection and 315 Korean control subjects in a pilot study.
Analysis of total pulmonary cytokine mRNA isolated 1 and 4 days following infection with rRSV/mIL-2 revealed elevated levels of mRNA for IL-2, gamma interferon (IFN-gamma), IL-4, IL-5, IL-6, IL-10, IL-13, and IL-12 p40 compared to those for wt rRSV.
Despite the increased IL-4 and IL-5 production and in contrast to mice primed with VV-G, mice primed with VV-Ftm(-) developed RSV-specific cytotoxic T lymphocytes (CTL) and maintained high levels of gamma interferon production.
Lung eosinophilia was also associated with a localized reduction in IFN-gamma and increased IL-4 and IL-5 mRNA transcription as well as elevated RSV specific IgG1 antibody production.
Also, adhesion of phytohaemagglutinin-activated tonsillar lymphocytes (TL) to RSV-infected epithelial cells caused a significant increase in interleukin (IL)-4 or IL-5 production.