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大鼠酵母聚糖诱导性胸膜炎中炎性细胞因子的产生:肿瘤坏死因子在体内诱导白细胞介素-6和细胞因子诱导的中性粒细胞趋化因子(CINC)。

Generation of inflammatory cytokines in zymosan-induced pleurisy in rats: TNF induces IL-6 and cytokine-induced neutrophil chemoattractant (CINC) in vivo.

作者信息

Utsunomiya I, Ito M, Oh-ishi S

机构信息

Department of Pharmacology, School of Pharmaceutical Sciences, Kitasato University, Tokyo, Japan.

出版信息

Cytokine. 1998 Dec;10(12):956-63. doi: 10.1006/cyto.1998.0376.

Abstract

Levels of inflammatory cytokines tumour necrosis factor (TNF), interleukin 1 (IL-1), IL-6, and cytokine-induced neutrophil chemoattractant (CINC), which is a member of the alpha-chemokine family in rats, were measured in the pleural exudates during zymosan-induced pleurisy to examine the relationship between the local production of cytokines and the inflammatory reaction. All four cytokine levels in the pleural exudate began to increase after 1-2 h, preceding the influx of neutrophils, and peaked after 4-5 h. Thereafter, these cytokine levels declined after 24 h, whereas the exudate volume still continued to increase and leukocyte number reached a plateau. Concomitant injection of actinomycin D (10 microg) with zymosan markedly suppressed the neutrophil infiltration, parallel with CINC production in the pleural exudate at 4 h. A transient elevation of IL-6 level, peaking at 5 h, and subsequent rise in the level of an acute-phase protein, T-kininogen, were also observed in the plasma. When recombinant human TNF-alpha (rhTNF-alpha) (20 000 U) was intrapleurally injected a rapid increase in pleural CINC level, followed by neutrophil infiltration, and a sharp rise in IL-6 level in the plasma, followed by an increase in T-kininogen, were demonstrated. These results suggest that CINC produced in the pleural exudate may participate in neutrophil infiltration, that IL-6 induced in the plasma stimulates T-kininogen production, and that endogenous TNF may be partly involved in the induction of CINC and IL-6 in this zymosan inflammation.

摘要

在酵母聚糖诱导的胸膜炎过程中,检测胸膜渗出液中炎性细胞因子肿瘤坏死因子(TNF)、白细胞介素1(IL-1)、IL-6以及细胞因子诱导的中性粒细胞趋化因子(CINC,大鼠α-趋化因子家族的一员)的水平,以研究细胞因子的局部产生与炎症反应之间的关系。胸膜渗出液中所有四种细胞因子水平在1-2小时后开始升高,早于中性粒细胞的流入,并在4-5小时后达到峰值。此后,这些细胞因子水平在24小时后下降,而渗出液体积仍继续增加,白细胞数量达到平台期。与酵母聚糖同时注射放线菌素D(10微克)可显著抑制中性粒细胞浸润,与4小时时胸膜渗出液中CINC的产生平行。在血浆中还观察到IL-6水平短暂升高,在5小时达到峰值,随后急性期蛋白T-激肽原水平升高。当胸膜腔内注射重组人TNF-α(rhTNF-α)(20000 U)时,胸膜CINC水平迅速升高,随后中性粒细胞浸润,血浆中IL-6水平急剧上升,随后T-激肽原增加。这些结果表明,胸膜渗出液中产生的CINC可能参与中性粒细胞浸润,血浆中诱导的IL-6刺激T-激肽原产生,内源性TNF可能部分参与这种酵母聚糖炎症中CINC和IL-6的诱导。

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