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Depressing hepatic macrophage complement receptor function causes increased susceptibility to endotoxemia and
Infection and Immunity
|March 1, 1985
Summary
Impaired hepatic macrophage complement receptor function, induced by immunoglobulin G (IgG) coated erythrocytes, increases susceptibility to endotoxin shock and bacterial infection in rats, highlighting its importance in host defense.
Area of Science:
- Immunology
- Pathophysiology
- Host Defense Mechanisms
Background:
- Previous studies indicated that thermal injury depresses in vivo hepatic macrophage complement receptor clearance function.
- The significance of this impaired complement receptor function in host defense remains to be fully elucidated.
Purpose of the Study:
- To investigate the impact of depressed complement receptor function on susceptibility to endotoxin shock and bacterial infection in uninjured animals.
- To determine if complement receptor impairment is a critical factor in host defense.
Main Methods:
- Hepatic complement receptor clearance function was assessed by measuring the uptake of immunoglobulin M (IgM) or immunoglobulin G (IgG) coated erythrocytes in rats.
- Depression of this function was induced by injecting varying doses of IgG-coated erythrocytes (EIgG).
- Susceptibility to endotoxin shock and Pseudomonas aeruginosa infection was evaluated following EIgG administration.
Main Results:
- Injection of higher doses of EIgG (8.7 X 10(8) or 17.4 X 10(8)/100 g) significantly depressed hepatic complement receptor clearance function.
- This depression was not attributable to reduced hepatic blood flow or C3 depletion.
- Increased susceptibility to endotoxin shock and P. aeruginosa infection correlated with the dose of EIgG administered.
Conclusions:
- Depression of hepatic macrophage complement receptor clearance function, induced by EIgG, compromises host defense.
- Impaired complement receptor function is a significant factor in increased susceptibility to endotoxin shock and bacterial infections.