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感染、外伤及恶性疾病可使体内产生白细胞介素-1(IL-1)和肿瘤坏死因子(TNF),这两种介质是由单核吞噬细胞产生的,刺激物包括细菌、内毒素及活性化补体 C5a 等。其中内毒索最强,在体外仅用微量(ng/ml)即可使人末梢血单核细胞同时诱导产生 IL-1a 和 TNF。内毒素产生的细胞分裂索与 C5a 有明显的诱导作用,亦即感染后使补体活化,虽少量内毒素对健康人的机体影响不大,但与 C5a 有增强作用,能够产生大量的细胞分裂素。IL-1a 及 TNF 循环到全身各脏器,引起非特异性炎症反应,急性反应期的临床表现为发热、嗜睡、食欲不振、末梢血白细胞增多、血沉增快、负氮平衡、C 反应蛋白和纤维蛋白原等急性期蛋白增高,以及高球蛋白血症等。虽然急性期机体的内环境对侵袭具有保护作用,但 IL-1和 TNF 能使体内发生不利的病理改变。在兔体内同时静注 IL-1和 TNF,使之产生类似败血症休克的循环状态,其机理可能与 IL-1及 TNF刺激中性白细胞和血管内皮细胞释放前列腺素等介质有关。IL-1/TNF 可使兔末梢血的白细胞和血小板
Infections, traumas, and malignancies produce interleukin-1 (IL-1) and tumor necrosis factor (TNF) in the body, both produced by mononuclear phagocytes, including bacteria, endotoxins, and activity Complement C5a and so on. The strongest endotoxin, in vitro with only trace (ng / ml) to make both peripheral blood mononuclear cells induced IL-1a and TNF. Endotoxin-induced cell division cable and C5a have a significant induction, that is, infection after complement activation, although a small amount of endotoxin on human health little effect, but with C5a have an enhanced role, can produce a large amount of cytokinin . IL-1a and TNF are circulated to various organs of the body and cause nonspecific inflammatory reactions. The clinical manifestations of acute reaction include fever, lethargy, loss of appetite, peripheral leukocytosis, rapid erythrocytosis, negative nitrogen balance, C-reactive protein and fiber Protein and other acute phase of protein increased, and hypergammaglobulinemia. Although the internal environment of the acute phase of the body has a protective effect against invasion, IL-1 and TNF can cause adverse pathological changes in vivo. The simultaneous intravenous injection of IL-1 and TNF in rabbits resulted in a cycle-like state similar to septic shock. The mechanism may be related to IL-1 and TNF-stimulated release of prostaglandin by neutrophils and vascular endothelial cells. IL-1 / TNF can make peripheral blood leukocytes and platelets in rabbits