Contribution of tumor necrosis factor α and interleukin-1 α on the production of macrophage inflammatory protein-2 in response to respiratory syncytial virus infection in a murine macrophage cell line, RAW264.7
✍ Scribed by Sakai, Shinya; Ochiai, Hiroshi; Kawamata, Hiroshi; Kogure, Toshiaki; Shimada, Yutaka; Nakajima, Katsuhisa; Terasawa, Katsutoshi
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 72 KB
- Volume
- 53
- Category
- Article
- ISSN
- 0146-6615
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✦ Synopsis
The production of several inflammatory cytokines, such as murine macrophage inflammatory protein-2 (MIP-2), tumor necrosis factor (TNF), and interleukin (IL)-1, was investigated in response to respiratory syncytial virus (RSV) infection in a murine macrophage cell line, RAW264.7, with special reference to mutual relation of their productions. The kinetics of MIP-2 production showed a trend for a biphasic pattern, that is, MIP-2 levels became detectable from 2 h postinfection (p.i.) and increased markedly until 8 h p.i. Thereafter, this level fell to the same level until 16 h p.i. and then increased again. TNF ␣ was also detectable at 2 h p.i. and then increased sharply until 8 h p.i., when the peak level attained. Compared with the levels of MIP-2 and TNF ␣, that of IL-1 ␣/, especially IL-1 , was lower (ng versus pg/ml order). The presence of anti-TNF ␣ or anti-IL-1 ␣ antibody did not influence the early phase of MIP-2 production but significantly inhibited the late phase, suggesting that MIP-2 is induced by the combined effects of RSV infection via direct induction and indirectly after initial induction of TNF ␣ and IL-1 ␣ productions. Although RSVinfected RAW264.7 cells had no alteration in viability compared with mock-infected control, these data demonstrate that RSV is a potent inducer of inflammatory cytokines by direct induction and indirectly via the initial production of other cytokines.