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KMID : 0357119940160030227
Korean Journal of Immunology
1994 Volume.16 No. 3 p.227 ~ p.236
The Role of Interferon-¥ã and Prostaglandin E2 in the Production of Tumor Necrosis Factor-¥á Mouse Macrophages Stimulated with Lipopolysaccharide
Kim Joong-Gon

Abstract
The roles of interferon-¥ãand prostaglandin E2 in the regulation of tumor necrosis factor-¥áproduction by mouse peritoneal macrophages stimulated with lipopolysaccharide were investigated. The production of TNF-¥á by mouse macrophages stimulated with LPS reached the peak level 3-6 hours after the in- itiation of culture and then rapidly decreased with time. IFN-¥ã increased the amount of and prolonged the duration of the production of TNF-¥á by macrophages in response to LPS. However, this enhancing effects of INF-¥á were not observed if IFN-¥ã were given to the macrophages 2 hours after the addition of LPS, suggesting that macropahges activated with LPS became resistant to enhancing effects of IFN-¥ã. PGE2 suppressed the production of TNF-¥á by macrophages stimulated with LPS, but IFN-¥ã reduced the suppressive effects of PGE2 on the TNF-¥á production by having macrophages resistant to the suppressive effect of PGE. Indomethacin, inhibitor of cyclooxygenase, enhanced the production of TNF-¥á in response to LPS or LPS and IFN-¥ã, suggesting that the endogenous PGE2 produced by macrophage stimulated with LPS might play a role in the suppression of TNF-¥á production in response to LPS. Collectively, the balance between the up-regulatory effect of IFN-¥ãproduced by T lymphocytes and down-regulatory effect of PGE2 produced by macrophage might play an important role in regulating the production of TNF-¥á by mouse macrophages in response to LPS
KEYWORD
Mouse macrophage LPS TNF-¥á IFN-¥ã PGE2 indomethacin
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