Suppr超能文献

抗巨噬细胞血清对嗜中性多形核白细胞向炎症腹膜腔迁移的阻断作用。

Blockade by antimacrophage serum of the migration of PMN neutrophils into the inflamed peritoneal cavity.

作者信息

de Souza G E, Ferreira S H

出版信息

Agents Actions. 1985 Oct;17(1):97-103. doi: 10.1007/BF01966691.

Abstract

The effect of rat antimacrophage serum (rAMS) was tested on the influence of normal or thioglycollate-stimulated macrophage populations of the rat peritoneal cavity on the migration of polymorphonuclear neutrophils (PMN) induced by carrageenin, heterologous serum (rabbit) and sheep red blood cells. The rAMS used did not cross-react with PMN or lymphocytes nor did it affect circulating white cells, complement levels or lysed PMN present in the inflammatory exudate. It did, however, give a positive immunofluorescence reaction with resident and stimulated macrophages. The rAMS inhibited macrophage function as tested by sheep red blood cell phagocytosis in vivo and release of a PMN chemotactic factor(s) in vitro. Thioglycollate-stimulated peritoneal cavities showed an increased macrophage population and responded with increased PMN migration when challenged with heterologous serum or carrageenin, as compared with control rats. The presence of rat antimacrophage antibodies inhibited PMN migration induced by heterologous serum, sheep red blood cells and carrageenin. It is concluded that resident macrophages participate in the control of PMN migration to the site of an acute inflammation by acting as 'alarm cells' and triggering several defence mechanisms which ultimately protect the host from injurious stimuli.

摘要

检测了大鼠抗巨噬细胞血清(rAMS)对大鼠腹腔正常或经巯基乙酸盐刺激的巨噬细胞群体,对角叉菜胶、异种血清(兔)和绵羊红细胞诱导的多形核中性粒细胞(PMN)迁移的影响。所使用的rAMS与PMN或淋巴细胞无交叉反应,也不影响循环白细胞、补体水平或炎症渗出物中裂解的PMN。然而,它与驻留和受刺激的巨噬细胞产生阳性免疫荧光反应。通过体内绵羊红细胞吞噬试验和体外PMN趋化因子释放试验检测,rAMS抑制巨噬细胞功能。与对照大鼠相比,经巯基乙酸盐刺激的腹腔巨噬细胞群体增加,在用异种血清或角叉菜胶攻击时PMN迁移增加。大鼠抗巨噬细胞抗体的存在抑制了异种血清、绵羊红细胞和角叉菜胶诱导的PMN迁移。得出的结论是,驻留巨噬细胞通过充当“警报细胞”并触发多种防御机制,参与控制PMN向急性炎症部位的迁移,这些机制最终保护宿主免受有害刺激。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验