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

1)婴儿和原发性呼吸道患儿鼻咽分泌物中细胞因子（IL-6和tnf - α）的活性。合胞病毒感染。在感染过程中，IL-6和tnf - α分别在100%和67%的病例中检测到。一般情况下，急性期tnf - α高，急性期后下降。IL-6活性在急性期最高，随后在5个月以下的婴儿中下降，在5个月以上的患者中呈白色，在疾病过程中升高，在早期恢复期达到峰值。不同年龄组的婴儿和儿童细胞因子的诱导机制可能不同。2)研究了新生儿（脐带血）和成人血单核细胞源性巨噬细胞（MDM）体外感染RSV后IL-6和tnf - α的产生及其mRNA的表达。脐带血MDM在感染后24小时内产生高水平的IL-6。在24-48小时和灭活病毒体外刺激后，检测到少量或不产生IL-6。与脐带血MDM不同，成人MDM在感染活RSV和暴露于灭活病毒24小时后显示出显著的IL-6活性。RSV感染后脐带血和成人血MDM产生tnf - α的模式与IL-6产生的模式相似。mRNA的表达谱与IL-6或tnf - α的产生相似。RSV感染后，新生儿细胞诱导IL-6产生的效率可能较低。3) RSV暴露后，新生儿MDM能够快速产生和分泌IL-6和tnf - α，而IL-12和ifn - α mRNA在RSV感染后显著表达，但不能产生。新生儿或婴幼儿呼吸道合胞病毒疾病的发病机制可能与这些细胞因子的产生模式部分相关。

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.