THE EFFECT OF INFLAMMATORY CYTOKINE AND APOPTOSIS ON PATHOGENESIS OF RSV INFECTION OF CHILDREN

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1) The cytokine (IL-6 and TNF-alpha) activity in nasopharyngeal secretions of infants and children with primary respiratory. syncytial virus (RSV) infection. IL-6 and TNF-alpha were detectable in 100% and 67% of cases during the course of infection, respectively. Generally, TNF-alpha was high in the acute phase and declined thereafter. IL-6 activity was also highest in the acute phase and declined thereafter in infants younger than 5 months, white in patients older than 5 months, it increased during the course of the disease to peak in the early convalescent phase. The mechanism of induction of cytokines may be differerent for infants and children in diffent age groups.2) The production of IL-6 and TNF-alpha and the expression of their mRNA were studied neonatal (cord blood) and adult blood monocyte-derived macrophages (MDM) after in vitro infection with RSV.Cord blood MDM exhibited production of high levels of IL-6 within 24 hr after infection. Little or no IL-6 production was detected after 24-48 hr and after in vitro stimulation with inactivated virus. Unlike cord blood MDM,adult MDM demonstrated significant activity of IL-6 after 24 hr infection with live RSV and after exposure to the inactivated virus. The pattern of TNF-alpha production by cord blood and adult blood MDM after live RSV infection resembled closely to the pattern of IL-6 production. The profile of mRNA expression was similar to the production of IL-6 or TNF-alpha. Neonatal cells may be less efficinet in inducing IL-6 production after RSV infection.3) Neonatal MDM can quick produce and secrete IL-6 and TNF-alpha after RSV exposure : however, it can not produce IL-12 and IFN-alpha in spite of the significant expression of there mRNA after RSV infection. Pathogenesis of RSV disease in neonates or young infants may be in partly correlated with these pattern of cytokines production.