Acute inflammation in gram-negative infection: endotoxin, interleukin 1, tumor necrosis factor, and neutrophils.
Acute inflammation in gram-negative infection: endotoxin, interleukin 1, tumor necrosis factor, and neutrophils.
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发表时间：
1987
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通讯作者：
H. Movat;M. Cybulsky;I. Colditz;Chan Mk;C. Dinarello
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作者：
H. Movat;M. Cybulsky;I. Colditz;Chan Mk;C. Dinarello
革兰氏阴性微生物诱导的真皮实验性细菌感染与急性炎症反应相关，这代表了对抗感染扩散的主要局部防御。当用放射性标记的细胞和蛋白质定量炎症反应时，动力学类似于用其他试剂（如免疫复合物或趋化因子）诱导的急性炎症。炎症反应的成分或事件之间存在相互关系;由于血管损伤是嗜中性粒细胞依赖性的，中性粒细胞必须迁移到细菌繁殖的部位。在贫血动物中，没有这种迁移，细菌增殖也没有受到抑制。这些微生物释放内毒素，进而诱导白细胞介素1（IL 1）和可能的肿瘤坏死因子的分泌。内毒素是能够诱导中性粒细胞内流的最有效的试剂（10（-15）mol vs. 10（-12）mol C5 ades Arg）。组织（可能是毛细血管后微静脉内皮）对IL 1的脱敏或快速耐受似乎控制了中性粒细胞流入的停止（也有体外证据）。嗜中性粒细胞对细菌的吞噬作用与嗜中性粒细胞释放氧自由基和溶酶体蛋白酶有关。这些都有助于引发微血管损伤，其特征在于增强的血管通透性，出血和血栓形成。
Experimental bacterial infection of the dermis induced with gram-negative microorganisms is associated with an acute inflammatory reaction, which represents the principal local defense against spread of the infection. When the inflammatory reaction is quantitated with radiolabeled cells and proteins, the kinetics resemble acute inflammation induced with other agents, such as immune complexes or chemotaxins. There is an interrelationship between the components or events of the inflammatory reaction; inasmuch as vascular injury is neutrophil-dependent, neutrophils must migrate to the site where the bacteria multiply. In neutropenic animals there is no such emigration and bacterial multiplication is not inhibited. The microorganisms shed endotoxin, which in turn induces secretion of interleukin 1 (IL 1) and probably tumor necrosis factor. Endotoxin is the most potent agent (10(-15) mol vs. 10(-12) mol of C5ades Arg) capable of inducing a neutrophil influx. Desensitization or tachyphylaxis of the tissues (probably of postcapillary venular endothelium) to IL 1 seems to control cessation of the neutrophil influx (also in vitro evidence). Phagocytosis of the bacteria by neutrophils is associated with release of oxygen radicals and lysosomal proteases from the neutrophils. These are instrumental in eliciting microvascular injury, which is characterized by enhanced vasopermeability, hemorrhage, and thrombosis.