書誌事項
- タイトル別名
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- Enhancement of Fas-mediated apoptosis in human neutrophils by a selective cyclaoxygenase-2 inhibitor
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Previous studies have shown that apoptosis of neutrophils represents a physiologic clearance mechanism in the circulation and in the tissue to create and maintain homeostasis of neutrophil numbers. It is well known that spontaneous and Fas-mediated apoptosis of neutrophils can be regulated by proinflammatory mediators. The effects of a selective cyclooxygenase-2 (COX-2) inhibitor, NS-398, on the Fas-mediated apoptosis in inflammatory stimuli-activated neutrophils were examined. Tumor necrosis factor-α(TNF-α) and granulocyte-macrophage stimulating factor (GM-CSF) enhanced PGE2 release through induction of COX-2, but not interleukin-1β(IL-1β) and IL-8. TNF-α- and GM-CSF-induced PGE2 release was abolished by the addition of NS-398 (1 μM), nevertheless NS-398 did not change the TNF-α- and GM-CSF-induced expression of COX-2. Although not only GM-CSF but also IL-1β and IL-8 delayed Fas-mediated apoptosis in neutrophils, this effect was suppressed by the addition of NS-398 (100 μM). On the contrary, TNF-α-treated neutrophils did not change the susceptibility to Fas-mediated apoptosis. These results suggest that selective COX-2 inhibitor not only suppresses PGE2 release, but also enhances Fas-mediated apoptosis of cytokine activated-neutrophils. Recent studies have provided evidence that COX-2 inhibitor acts through a COX-2-independednt mode of various cell functions. Therefore, the proapoptotic activity of selective COX-2 inhibitor may be independent of COX-2 activity. Considering these studies, selective COX-2 inhibitor may contribute to come to an end of acute inflammation via enhanced apoptosis of neutrophils.
収録刊行物
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- 炎症・再生
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炎症・再生 23 (3), 175-180, 2003
一般社団法人 日本炎症・再生医学会
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詳細情報 詳細情報について
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- CRID
- 1390001205178786816
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- NII論文ID
- 130000165310
- 80015961042
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- NII書誌ID
- AA11508953
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- ISSN
- 18805795
- 13468022
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可