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
Cunha, FQ
中科院分区:
医学2区
文献类型:
--
作者:
Bombini, G;Canetti, C;Cunha, FQ

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肿瘤坏死因子(TNF)-α、白细胞介素-1 β、白细胞介素-8和白三烯B-4在免疫炎症过程中对中性粒细胞募集具有重要作用。在这里,我们评估了几种炎症介质对免疫大鼠膝关节间隙中卵清蛋白诱导的中性粒细胞募集的参与。卵清蛋白给药在免疫大鼠中诱导了剂量和时间依赖性的中性粒细胞聚集,地塞米松、戊茶碱或沙利度胺可抑制该聚集,但选择性一氧化氮抑制剂不能抑制该聚集(硝基-L-精氨酸),血小板活化因子(BN 50730或UK 74505)、异甘草素(吲哚美辛)、组胺(甲氯新)或白三烯B-4(MK 886和CP 105,696)。抗TNF-α抗血清,而非抗白细胞介素-1 β或抗CINC-1(白细胞介素诱导的中性粒细胞趋化因子1)抗血清,可损害卵清蛋白诱导的中性粒细胞蓄积。在渗出液中检测到大量的TNF-α,其被地塞米松、戊茶碱和沙利度胺抑制。这些结果表明TNF-α在该模型中的特定作用,并且喷替福林和沙利度胺抑制中性粒细胞流入和TNF-α释放的能力可能在关节炎中具有治疗意义。(C)2004 Elsevier B. V.保留所有权利。
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.