Movat H Z, Cybulsky M I, Colditz I G, Chan M K, Dinarello C A
Fed Proc. 1987 Jan;46(1):97-104.
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.
由革兰氏阴性微生物引起的真皮实验性细菌感染与急性炎症反应相关，这种反应是针对感染扩散的主要局部防御机制。当用放射性标记的细胞和蛋白质对炎症反应进行定量时，其动力学类似于由其他因子（如免疫复合物或趋化因子）诱导的急性炎症。炎症反应的各个组成部分或事件之间存在相互关系；由于血管损伤依赖于中性粒细胞，中性粒细胞必须迁移到细菌繁殖的部位。在中性粒细胞减少的动物中，不存在这种迁移，细菌繁殖也不会受到抑制。微生物释放内毒素，内毒素反过来又诱导白细胞介素1（IL 1）的分泌，可能还诱导肿瘤坏死因子的分泌。内毒素是能够诱导中性粒细胞流入的最有效因子（10^(-15)摩尔对10^(-12)摩尔的C5ades 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（体外实验也有证据）。中性粒细胞对细菌的吞噬作用与中性粒细胞释放氧自由基和溶酶体蛋白酶有关。这些物质有助于引发微血管损伤，其特征是血管通透性增加、出血和血栓形成。
