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Infect Immun. 1985 March; 47(3): 659-664

Depressing hepatic macrophage complement receptor function causes increased susceptibility to endotoxemia and infection.

ABSTRACT

Previous work has demonstrated that in vivo hepatic macrophage complement receptor clearance function is depressed after thermal injury. To determine whether impairment of complement receptor function is important in host defense, the present study evaluated the effect of the depression of complement receptor function in uninjured animals on susceptibility to endotoxin shock and bacterial infection. Hepatic complement receptor clearance function was evaluated by measuring the hepatic uptake of a test dose (2.9 X 10(8)/100 g) of rat erythrocytes coated with anti-erythrocyte immunoglobulin M (EIgM) or EIgG in rats. Depression of hepatic complement receptor function was induced by the injection of EIgG. The hepatic uptake of the test dose of EIgM or EIgG was depressed after the injection of 8.7 X 10(8) EIgG per 100 g and 17.4 X 10(8) EIgG per 100 g but not after the injection of 2.9 X 10(8) EIgG per 100 g. This effect was shown not to be due to a decrease in hepatic blood flow or a depletion of serum C3 and was, therefore, due to a depression in hepatic macrophage complement receptor clearance function. Susceptibility to endotoxin shock was increased with the dose of 8.7 X 10(8) EIgG per 100 g, and susceptibility to infection with Pseudomonas aeruginosa was increased with the dose of 17.4 X 10(8) EIgG per 100 g. Therefore, depression of hepatic macrophage complement receptor clearance function with EIgG is associated with depressed host defense.

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