Innate host-defensive function of a hepatic lipid fraction produced in low-dose carbon tetrachloride-pretreated mice.

We investigated the tolerance of mice to carbon tetrachloride (CCl(4))-induced fulminant hepatic failure (FHF) in mice with daily intraperitoneal (i.p.) injection of high-dose CCl(4) (4 ml/kg). The tolerance was induced by preliminary i.p. administration of a low dose of CCl(4) (1 ml/kg) 24 h prior to the initial high-dose administration of CCl(4) (4 ml/kg). These mice were protected from death because of FHF induced by subsequent daily high-dose injection of CCl(4). This protection appears to result from a priming effect of the innate immune activity of CCl(4). The crude lipid extracted from the liver of low-dose CCl(4) injected mice also protected mice from death because of FHF. Examination of the innate immunological system using OK-432 (picibanil) revealed that the protection results from a priming effect of the innate immune activity with the low-dose CCl(4) or the crude lipid extract.