Abstract
When human hepatocytes were incubated with low concentrations of ethanol they general chemotactic activity for human neutrophils. Generation of chemotactic activity was dependent upon duration of incubation and concentration of ethanol used. Production of chemotactic activity by ethanol-treated hepatocytes was inhibited completely in the presence of the alcohol dehydrogenase inhibitor 4-methylpyrazole. PMN isolated from rats, in contrast, do not respond chemotactically to the factor released by homologous cells. Preliminary studies indicated that the chemotactic factor is non-polar in nature (perhaps related to leukotriene B 4). These results indicate that human hepatocytes, when exposed to ethanol, generate chemotactic factor(s) for human PMN. The occurence of this phenomenon may explain, in part, the PMN infiltrates observed in human liver during the course of acute alcoholic hepatitis.
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