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[发热状态:体液和细胞因子]

[Status febrilis: humoral and cellular factors].

作者信息

Block L H

出版信息

Schweiz Med Wochenschr. 1980 Mar 22;110(12):430-7.

PMID:7394469
Abstract

Clinical fever seems clearly associated with those diseases in which inflammation, in one form or other, plays a dominant role. The actual contribution of the various listed factors to the febrile response associated with any specific disease may, of course, be complex. For instance in a gram-positive infection, inflammatory cells may be activated to produce endogenous pyrogen at the site of bacterial multiplication by any or all of the following mechanisms, most of which have been demonstrated experimentally: phagocytosis of bacteria, chemotactic factors produced by bacteria or released from injured tissue of complement activation, immune reactions (either cellular or antibody-mediated) in a previously sensitized host, and toxins, e.g. endotoxins which may activate phagocytic cells directly.

摘要

临床发热似乎明显与那些炎症以某种形式起主导作用的疾病相关。当然,各种所列因素对与任何特定疾病相关的发热反应的实际作用可能很复杂。例如,在革兰氏阳性菌感染中,炎症细胞可能通过以下任何一种或全部机制被激活,在细菌繁殖部位产生内源性致热原,其中大多数已通过实验得到证实:细菌的吞噬作用、细菌产生的或从补体激活的受损组织释放的趋化因子、先前致敏宿主中的免疫反应(细胞介导或抗体介导)以及毒素,例如可直接激活吞噬细胞的内毒素。

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