Reactive oxidants mediate TNF-alpha-induced leukocyte adhesion to rat mesenteric venular endothelium.
Reactive oxidants mediate TNF-alpha-induced leukocyte adhesion to rat mesenteric venular endothelium.
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反应性氧化剂介导 TNF-α 诱导的白细胞与大鼠肠系膜小静脉内皮的粘附。
DOI：
10.1152/ajpheart.1995.269.6.h1833
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Bulkley,GB
中科院分区：
文献类型：
--
作者：
Morita,Y;Clemens,MG;Miller,LS;Rangan,U;Kondo,S;Miyasaka,M;Yoshikawa,T;Bulkley,GB
我们使用活体显微镜和固定的肠系膜整体制剂，研究了活性氧代谢物（ROM）作为肿瘤坏死因子-α（TNF-α）刺激的中性粒细胞体内粘附到大鼠肠系膜小静脉的潜在介质的作用。腹腔注射TNF-α以剂量和时间依赖性方式显着增加白细胞滚动、粘附和迁移。事先静脉注射单克隆抗细胞间粘附分子-1 (ICAM-1) 可显着减弱白细胞粘附和迁移，但不会减弱白细胞滚动。静脉内预给予超氧化物歧化酶（SOD）、过氧化氢酶或两者均显着减弱滚动白细胞通量。只有过氧化氢酶或SOD加过氧化氢酶才能显着抑制白细胞粘附。过氧化氢酶单独抑制迁移。此外，TNF-α给药后4小时，用过氧化氢酶而不是SOD进行粘附后处理，减少了先前因响应TNF-α而增加的滚动（但不是粘附）白细胞的流量。胃内别嘌呤醇（50 mg/kg，TNF-α给药前3和18小时）或3周富含钨的饮食显着抑制黄嘌呤氧化酶活性，但对中性粒细胞动力学的上述参数没有显着影响。在使用专门针对中性粒细胞酯酶染色的阑尾系膜的固定整体制备物的平行实验中，连续静脉内施用过氧化氢酶也可抑制TNF-α施用后2小时的中性粒细胞粘附，但SOD、胃内别嘌呤醇或钨饮食则不会抑制该作用。这些发现表明，ROM（显然不是来自黄嘌呤氧化酶）是 TNF-α 诱导的大鼠肠系膜微静脉中性粒细胞粘附上调的重要介质。
We investigated the role of reactive oxygen metabolites (ROMs) as potential mediators of tumor necrosis factor-alpha (TNF-alpha)-stimulated neutrophil adhesion to rat mesenteric venules in vivo, using intravital microscopy and fixed whole mount preparations of mesentery. Intraperitoneal injection of TNF-alpha significantly increased leukocyte rolling, adhesion, and emigration in a dose- and time-dependent manner. Leukocyte adhesion and emigration, but not rolling, were significantly attenuated by prior intravenous administration of monoclonal anti-intercellular adhesion molecule-1 (ICAM-1). Rolling leukocyte flux was significantly attenuated by intravenous preadministration of superoxide dismutase (SOD), catalase, or both. Only catalase or SOD plus catalase significantly inhibited leukocyte adhesion. Catalase alone inhibited emigration. Moreover, postadhesive treatment with catalase but not SOD, 4 h after TNF-alpha administration reduced the flux of rolling (but not adherent) leukocytes that had previously increased in response to TNF-alpha. Intragastric allopurinol (50 mg/kg at 3 and 18 h before TNF-alpha administration) or 3 wk of a tungsten-enriched diet substantially inhibited xanthine oxidase activity but had no significant effects on the above parameters of neutrophil dynamics. In parallel experiments using fixed whole mount preparations of the mesoappendix stained specifically for neutrophil esterase, neutrophil adhesion 2 h after TNF-alpha administration was also inhibited by continuous intravenous administration of catalase but not by SOD, intragastric allopurinol, or tungsten diet. These findings suggest that ROMs, apparently not from xanthine oxidase, are important mediators of TNF-alpha-induced upregulation of neutrophil adhesion in rat mesenteric venules.