STAPHYLOCOCCUS-EPIDERMIDIS INDUCES COMPLEMENT ACTIVATION, TUMOR-NECROSIS-FACTOR AND INTERLEUKIN-1, A SHOCK-LIKE STATE AND TISSUE-INJURY IN RABBITS WITHOUT ENDOTOXEMIA - COMPARISON TO ESCHERICHIA-COLI
STAPHYLOCOCCUS-EPIDERMIDIS INDUCES COMPLEMENT ACTIVATION, TUMOR-NECROSIS-FACTOR AND INTERLEUKIN-1, A SHOCK-LIKE STATE AND TISSUE-INJURY IN RABBITS WITHOUT ENDOTOXEMIA - COMPARISON TO ESCHERICHIA-COLI
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DOI：
10.1172/jci115218
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发表时间：
1991-06-01
影响因子：
15.9
通讯作者：
DINARELLO, CA
中科院分区：
文献类型：
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作者：
WAKABAYASHI, G;GELFAND, JA;DINARELLO, CA
肿瘤坏死因子（TNF）和IL-1被认为介导了内毒素血症和革兰氏阴性菌血症的许多病理生理变化。 在这些研究中，将热灭活的表皮葡萄球菌输注到家兔体内，以确定不含内毒素（LPS）的微生物是否也会引起细胞因子血症和革兰氏阴性菌血症中观察到的生理异常。 S.表皮葡萄球菌引起的补体激活、循环TNF和IL-1以及低血压的程度与热灭活大肠杆菌的二十分之一相同。 循环中IL-1-β水平与低血压程度的相关系数（r = 0.81，P <0.001）大于TNF水平（r = 0.48，P <0.02）。 白细胞减少症、血小板减少症、弥漫性肺毛细血管中性粒细胞聚集和肝坏死伴中性粒细胞浸润在两种S. epidermidis或E.大肠杆菌输注。 然而，S. epidermidis输注未引起明显的内毒素血症（<60 pg/ml），而E.大肠杆菌输注导致高（11，000 pg/ml）血清内毒素水平。 S. epidermidis、E. coli、LPS或S.表皮衍生的脂磷壁酸（LTA）在体外诱导血液单个核细胞产生TNF和IL-1。 e.大肠杆菌和LPS的效力比S.表皮或LTA。 因此，在S. epidermidis或E.杆菌 这些数据提供了进一步的证据，宿主因子如IL-1和TNF是感染性休克综合征的常见介质，无论生物体如何。
Tumor necrosis factor (TNF) and IL-1 are thought to mediate many of the pathophysiologic changes of endotoxemia and Gram-negative bacteremia. In these studies, heat-killed Staphylococcus epidermidis were infused into rabbits to determine whether an endotoxin (LPS)-free microorganism also elicits cytokinemia and the physiologic abnormalities seen in Gram-negative bacteremia. S. epidermidis induced complement activation, circulating TNF and IL-1, and hypotension to the same degree as did one-twentieth the number of heat-killed Escherichia coli. Circulating IL-1-beta levels had a greater correlation coefficient (r = 0.81, P < 0.001) with the degree of hypotension than TNF levels (r = 0.48, P < 0.02). Leukopenia, thrombocytopenia, diffuse pulmonary capillary aggregation of neutrophils, and hepatic necrosis with neutrophil infiltration were observed to the same extent after either S. epidermidis or E. coli infusion. However, S. epidermidis infusion did not induce significant (< 60 pg/ml) endotoxemia, whereas E. coli infusion resulted in high (11,000 pg/ml) serum endotoxin levels. S. epidermidis, E. coli, LPS, or S. epidermidis-derived lipoteichoic acid (LTA) induced TNF and IL-1 from blood mononuclear cells in vitro. E. coli organisms and LPS were at least 100-fold more potent than S. epidermidis or LTA. Thus, a shock-like state with similar levels of complement activation as well as circulating levels of IL-1 and TNF were observed following either S. epidermidis or E. coli. These data provide further evidence that host factors such as IL-1 and TNF are common mediators of the septic shock syndrome regardless of the organism.