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[乙醛诱导的酒精性肝病中白细胞迁移抑制]

[Acetaldehyde-induced leukocyte migration inhibition in alcoholic liver diseases].

作者信息

Nilius R, Königstedt B, Zipprich B, Busse H J, Lorenz G

出版信息

Z Gesamte Inn Med. 1982 Jun 15;37(12):393-7.

PMID:7124038
Abstract

Acetaldehyde in non-toxic doses (15.6 micrograms per start) causes in the inhibition test of the migration of leucocytes an inhibition of the migration in 6/13 of the patients with alcoholic hepatitis, a stimulation of the migration in 6/11 of alcohol cirrhoses. Healthy (n = 16) persons, patients with alcoholic fatty degeneration of the liver (n = 3) as well as non-alcoholic liver diseases (chronic persisting hepatitis, n = 11; chronic active hepatitis, n = 8, cirrhosis, n = 7) did not show this cellular immune reagibility. The inhibition of the migration and the stimulation of the migration, respectively, might develop by hapten autoantigen complexes (altered cytoskeleton?) with release of the factors of inhibition of migration and stimulation of migration, in which case the role of a hapten belongs to acetaldehyde. The results of the tests did not correlate with functional and histological findings of the liver, with the actual consumption of alcohol and also not with haptoglobin phaenotypes. When it is postulated that by acetaldehyde also the release of further lymphokines is mediated, origin and progression of alcoholic hepatitis and alcoholic cirrhosis might be explained immunopathogenetically.

摘要

无毒剂量的乙醛(每次起始剂量为15.6微克)在白细胞迁移抑制试验中,导致6/13的酒精性肝炎患者的白细胞迁移受到抑制,6/11的酒精性肝硬化患者的白细胞迁移受到刺激。健康人(n = 16)、酒精性脂肪肝患者(n = 3)以及非酒精性肝病患者(慢性持续性肝炎,n = 11;慢性活动性肝炎,n = 8,肝硬化,n = 7)均未表现出这种细胞免疫反应性。迁移抑制和迁移刺激可能分别由半抗原自身抗原复合物(改变的细胞骨架?)通过释放迁移抑制因子和迁移刺激因子而产生,在这种情况下,半抗原的作用属于乙醛。试验结果与肝脏的功能和组织学检查结果、实际酒精摄入量以及触珠蛋白表型均无相关性。如果假定乙醛还介导了其他淋巴因子的释放,那么酒精性肝炎和酒精性肝硬化的发生及进展可能可以从免疫病理学角度得到解释。

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