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Cytokine production of RSV/PHA-stimulated tonsillar mononuclear cells: influences of age and atopy

¹ University Medicine, Southampton General Hospital, Southampton and ² Dept of Respiratory Medicine, National Heart and Lung Institute and Wright Fleming Institute of Infection and Immunity, Faculty of Medicine, Imperial College, London, UK. ³ Chiba Prefectural Institute of Public Health, Chiba City, Japan

CORRESPONDENCE: S.L. Johnston, Dept of Respiratory Medicine, National Heart and Lung Institute and Wright Fleming Institute of Infection and Immunity, Imperial College, Norfolk Place, London, W2 1PG, UK. Fax: 44 2072628913. E-mail: s.johnston@ic.ac.uk

Keywords: allergic sensitisation, respiratory syncytial virus, T-helper cell type 1, T-helper cell type 2

Received: September 24, 2002
Accepted April 4, 2003

This study was supported by the British Lung Foundation, Garfield Weston Fellowship, grant number F96/09.

Links between immune responses to respiratory syncytial virus (RSV), age and atopic sensitisation are poorly understood.

This study investigated the induction of target organ type-1, type-2 and pro-inflammatory cytokine responses to RSV and/or phytohaemagglutinin (PHA) in tonsillar mononuclear cells from children, in relation to age and atopic status.

In comparison with the control medium, RSV induced production of the type-1 cytokines interferon (IFN)- and interleukin (IL)-18, the pro-inflammatory cytokines IL-6, -8 and RANTES (regulated on activation, normal T-cell expressed and secreted), but not any of the type-2 cytokines IL-4, -5, -10 and -13. Induction of IL-6, -8 and RANTES, but not IFN- or IL-18, were shown to be dependent on virus replication. PHA induced all except IL-12, -13, and -15. Induction of IFN-, IL-6, -8, and RANTES was significantly increased in atopic children. Induction of both IFN- andIL-4 increased in parallel in relation to age, with no change in the IFN-:IL-4 ratio.

These data are compatible with the hypothesis that immature type-1 immunity during early childhood plays a role in both respiratory syncytial virus bronchiolitis and in its relationship with atopy.