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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
Author(s) -
Sakai Shinya,
Ochiai Hiroshi,
Kawamata Hiroshi,
Kogure Toshiaki,
Shimada Yutaka,
Nakajima Katsuhisa,
Terasawa Katsutoshi
Publication year - 1997
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/(sici)1096-9071(199710)53:2<145::aid-jmv6>3.0.co;2-9
Subject(s) - tumor necrosis factor alpha , macrophage , macrophage inflammatory protein , cytokine , biology , virus , cell culture , immunology , interleukin , mononegavirales , virology , proinflammatory cytokine , inflammation , microbiology and biotechnology , paramyxoviridae , in vitro , viral disease , biochemistry , genetics
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 α 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 α, that of IL‐1 α/β, especially IL‐1 β, was lower (ng versus pg/ml order). The presence of anti‐TNF α or anti‐IL‐1 α 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 α and IL‐1 α productions. Although RSV‐infected RAW264.7 cells had no alteration inviability 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. J. Med. Virol. 53:145–149, 1997. © 1997 Wiley‐Liss, Inc.