INTERACTION OF KUPFFER CELLS TO SPLENIC MACROPHAGES AND HEPATOCYTES IN ENDOTOXIN CLEARANCE - EFFECT OF ALCOHOL
INTERACTION OF KUPFFER CELLS TO SPLENIC MACROPHAGES AND HEPATOCYTES IN ENDOTOXIN CLEARANCE - EFFECT OF ALCOHOL
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DOI：
10.1111/j.1440-1746.1995.tb01793.x
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发表时间：
1995-01-01
影响因子：
4.1
通讯作者：
TSUJII, T
中科院分区：
文献类型：
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作者：
FUKUI, H;KITANO, H;TSUJII, T
高剂量乙醇慢性酒精喂养大鼠的额外管理导致内毒素清除率下降，并伴随着门静脉中肿瘤坏死因子（TNF）水平升高的脾内毒素积累增加。慢性乙醇负荷大鼠枯否细胞（KC）和脾巨噬细胞的内毒素摄取和TNF产生均显著高于对照组。用含10 ~ 100 mmol/L乙醇的培养基预培养KC，可使KC摄取内毒素和产生TNF的能力降低。但这并不影响脾巨噬细胞的内毒素摄取和TNF的产生. KC在含乙醇的培养基中预孵育，并将所得培养上清加入肝细胞培养体系中，可增加肝细胞内毒素结合蛋白的产生.这种内毒素结合蛋白被证明可以增强KC对内毒素的摄取，并抑制KC中TNF的产生。当KC和肝细胞从慢性酒精喂养的大鼠分离，进一步添加乙醇的KC培养基中没有影响肝脏的内毒素结合蛋白的生产。肝内毒素结合蛋白产生的增加可能是对抗内毒素的一种防御机制。有一种可能性是，这种防御机制的损害在慢性酗酒者的内毒素血症和内毒素的发展中起着关键作用。
An additional administration of high dose ethanol to chronic alcohol-fed rats led to a decrease in endotoxin clearance and an increase in endotoxin accumulation in the spleen accompanied by an elevation of tumour necrosis factor (TNF) levels in the portal vein. Endotoxin uptake and TNF production by Kupffer cells (KC) and splenic macrophages in the chronic ethanol load rats were significantly greater than those in the control rats. When these cells were precultured in the medium containing 10 to 100 mmol/L ethanol, the endotoxin uptake and TNF production of KC were decreased. However, this did not affect the endotoxin uptake and TNF production of splenic macrophages.The hepatic production of endotoxin binding protein was increased when KC were preincubated in the medium containing ethanol and the resultant culture supernatant was added to the hepatocyte culture system. This endotoxin binding protein was proved to enhance the uptake of endotoxin and suppressed the production of TNF in the KC. When KC and hepatocytes were isolated from chronically alcohol-fed rats, further addition of ethanol to the culture medium of KC did not affect the hepatic production of endotoxin binding protein. The increase in hepatic production of endotoxin binding protein may serve as a defence mechanism against endotoxicity. There is a possibility that an impairment of this defence mechanism has a pivotal role in the development of endotoxaemia and endotoxicity in chronic alcoholics.