Respiratory syncytial virus triggers synthesis of IL-6 in BALB/c mouse alveolar macrophages in the absence of virus replication

被引:19
作者
Stadnyk, AW
Gillan, TL
Anderson, R
机构
[1] DALHOUSIE UNIV,DEPT MICROBIOL & IMMUNOL,HALIFAX,NS B3H 4H7,CANADA
[2] DALHOUSIE UNIV,DEPT PEDIAT,HALIFAX,NS B3H 4H7,CANADA
关键词
D O I
10.1006/cimm.1996.1075
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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-1 beta (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. (C) 1997 Academic Press.
引用
收藏
页码:122 / 126
页数:5
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