Tumour necrosis factor-α mediates neutrophil migration to the knee synovial cavity during immune inflammation
Tumour necrosis factor-α mediates neutrophil migration to the knee synovial cavity during immune inflammation
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DOI:
10.1016/j.ejphar.2004.06.003
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发表时间:
2004-08-02
影响因子:
5
通讯作者:
Cunha, FQ
中科院分区:
文献类型:
--
作者:
Bombini, G;Canetti, C;Cunha, FQ
Tumour necrosis factor (TNF)-alpha, interleukin-1beta, interleukin-8 and leukotriene B-4 have an important role on neutrophil recruitment during immune-inflammation. Here we evaluated the participation of several inflammatory mediators on ovalbumin-induced neutrophil recruitment in the knee articular space of immunized rats. Ovalbumin administration in immunized, but not in control, rats induced a dose- and time-dependent neutrophil accumulation, which was inhibited by dexamethasone, pentoxifylline or thalidomide, but not by selective inhibitors of nitric oxide (nitro-L-arginine), platelet-activating factor (BN50730 or UK74505), prostaglandins (indomethacin), histamine (meclisine) or leukotriene B-4 (MK 886 and CP105,696). Anti-TNF-alpha antiserum, but not anti-interleukin-1beta or anti-CINC-1 (cytokine-induced neutrophil chemoattractant 1) antisera, impaired ovalbumin-induced neutrophil accumulation. High amounts of TNF-alpha were detected in the exudates, which was inhibited by dexamethasone, pentoxifylline and thalidomide. These results suggest a specific role for TNF-alpha in this model, and the ability of pentoxifylline and thalidomide to inhibit both neutrophil influx and TNF-alpha release may have therapeutic implications in arthritis. (C) 2004 Elsevier B.V. All rights reserved.