清醒大鼠内毒素血症和革兰氏阴性败血症时肾白介素-1的表达。

Circulatory shock Pub Date : 1994-07-01
Z Laszik, T Nadasdy, L D Johnson, M R Lerner, D Brackett, F G Silva
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引用次数: 0

摘要

内毒素诱导的细胞因子,如白细胞介素-1 (IL-1)和肿瘤坏死因子(TNF)被认为有助于内毒素在革兰氏阴性感染中的促炎作用。采用LD95剂量内毒素(n = 24)或活大肠杆菌(E. coli) (n = 24)引起的脓毒症的意识大鼠模型,我们在不同时间间隔检查肾脏冷冻切片,以寻找IL-1 α和TNF α表达的证据。免疫组织化学方法显示,内毒素和大肠杆菌治疗的动物在脓毒症开始后30和90分钟,肾小球内皮细胞中有短暂的IL-1 α表达。免疫组化检测内皮细胞IL-1 α的表达与Northern blot检测IL-1 α mRNA的表达同时发生。通过萘酚as - d氯乙酸酯酶组织化学反应发现,肾小球内皮IL-1 α的表达与肾小球多形核白细胞数量的轻微但显著增加相一致。肾小球内皮IL-1 α在180分钟和360分钟内几乎没有表达。肾组织在任何时间间隔内均未检测到TNF α的表达。肾小球中未发现α -乙酸萘酯酶阳性或酸性磷酸酶阳性的单核/巨噬细胞。我们的研究结果提供了直接的体内证据,证明IL-1 α基因产物在脓毒症大鼠模型中通过肾小球内皮细胞在肾脏中局部表达。
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Renal interleukin-1 expression during endotoxemia and gram-negative septicemia in conscious rats.

Endotoxin-induced cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF) are thought to contribute to the proinflammatory effects of endotoxin in gram-negative infections. Using a conscious rat model of sepsis, induced by intravenous challenge with LD95 doses of endotoxin (n = 24) or live Escherichia coli (E. coli) (n = 24), we examined frozen sections of kidney at various intervals for evidence of IL-1 alpha and TNF alpha expression. A transient glomerular endothelial IL-1 alpha expression was demonstrated at 30 and 90 min after initiation of the sepsis in both endotoxin and E. coli-treated animals using immunohistochemistry. The endothelial IL-1 alpha expression as determined by immunohistochemistry occurred at the same time as IL-1 alpha mRNA expression, as determined by Northern blot analysis. The glomerular endothelial IL-1 alpha expression coincided with a slight but significant increase in the number of the glomerular polymorphonuclear leukocytes as identified by naphthol AS-D chloroacetate esterase enzyme histochemical reaction. Glomerular endothelial IL-1 alpha expression was virtually absent by 180 and 360 min. No TNF alpha expression was detected in the renal tissues at any time interval. Neither alpha-naphthyl acetate esterase-positive nor acid phosphatase-positive monocytes/macrophages were identified in the glomeruli. Our findings provide direct in vivo evidence that the IL-1 alpha gene product is expressed locally in the kidney by glomerular endothelial cells in this septic rat model.

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