In mice, respiratory syncytial virus (RSV) infection during allergic provocation aggravates the allergic Th2 immune response, characterised by production of interleukin (IL)-4, IL-5, and IL-13, and eosinophilic inflammation. This enhancement of the Th2 response occurs simultaneously with a strong RSV-induced Th1 cytokine response (IL-12 and IFN-γ). The present study investigated whether IFN-γ and IL-12 are critically involved in this RSV-enhanced OVA allergy. Therefore, IFN-γR- and IL-12-deficient mice (both on a 129/Sv/Ev background) were sensitised and challenged with ovalbumin (OVA) and infected with RSV during the OVA challenge period. Neither gene deletion affected the development of ovalbumin-induced allergic inflammation in mice. However, when OVA-allergic IFN-γR deficient mice were infected with RSV, an increased pulmonary eosinophilic infiltrate and increased IL-4 and IL-13 mRNA expression in lung tissue were observed compared with identically treated wild-type mice. In contrast, deficiency of IL-12 did not aggravate the Th2 immune and inflammatory response in OVA/RSV-treated mice, compared with wild-type. In conclusion, the virus-induced IFN-γ response diminishes the Th2 inflammatory response during OVA allergy but fails to prevent totally the enhancement of the OVA allergy by RSV. In contrast, IL-12 is not involved in inhibiting nor increasing the RSV-enhanced allergy in 129/Sv/Ev mice.

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Journal of Medical Virology
Department of Pediatrics

Barends, M, Boelen, A, de Rond, L.G.H, Dormans, J.A.M.A, Kwakkel, J, van Oosten, M, … Kimman, T.G. (2003). Respiratory syncytial virus enhances respiratory allergy in mice despite the inhibitory effect of virus-induced interferon-γ. Journal of Medical Virology, 69(1), 156–162. doi:10.1002/jmv.10252