Stadnyk A W, Gillan T L, Anderson R
Departments of Pediatrics, Dalhousie University, Halifax, Nova Scotia, Canada.
Cell Immunol. 1997 Mar 15;176(2):122-6. doi: 10.1006/cimm.1996.1075.
Cytokines produced by alveolar macrophages are likely involved in the regulation of the immune response arising from respiratory syncytial virus (RSV) infection. Both infectious and UV-inactivated RSV were effective in inducing BALB/c mouse alveolar macrophages to synthesize increased levels of IL-6 mRNA and secreted IL-6 protein. No increase in IL-1beta (either mRNA or secreted protein) was observed. The augmented production of IL-6 was activated by purified virus and was reduced by pretreating virus with virus-neutralizing antiserum, demonstrating a requirement for virus in the enhanced IL-6 response. The results suggest that the exposure of BALB/c alveolar macrophages to small quantities of RSV (in the absence of detectable virus replication) is sufficient to trigger IL-6 production. The finding that UV-inactivated virus was effective in triggering IL-6 production by mouse alveolar macrophages is similar to that reported in human alveolar macrophages, providing further validation of the BALB/c mouse as a useful animal model for human RSV infection.
肺泡巨噬细胞产生的细胞因子可能参与调节由呼吸道合胞病毒（RSV）感染引发的免疫反应。感染性RSV和紫外线灭活的RSV均可有效诱导BALB/c小鼠肺泡巨噬细胞合成水平升高的IL-6 mRNA并分泌IL-6蛋白。未观察到IL-1β（mRNA或分泌蛋白）增加。纯化病毒激活了IL-6的增加产生，而用病毒中和抗血清预处理病毒则使其减少，这表明增强的IL-6反应需要病毒。结果表明，BALB/c肺泡巨噬细胞暴露于少量RSV（在未检测到病毒复制的情况下）足以触发IL-6产生。紫外线灭活病毒能有效触发小鼠肺泡巨噬细胞产生IL-6这一发现与人类肺泡巨噬细胞的报道相似，进一步验证了BALB/c小鼠作为人类RSV感染有用动物模型的有效性。
