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Inhibition of Corynebacterium parvum‐primed and lipopolysaccharide‐induced hepatic necrosis in rats by selective depletion of neutrophils using a monoclonal antibody

To examine whether neutrophils are involved in the pathogenesis of experimental liver dysfunction, we observed the effect of selective in vivo neutrophil depletion by a monoclonal antibody (RP‐3) on the pathogenesis of acute experimental hepatic necrosis in rats induced by a preparative injection of heat‐killed Corynebacterium parvum and a challenging dose of lipopolysaccharide (LPS) (positive control group). The serum transaminase titer 8 h after LPS injection was reduced by selective depletion of peripheral blood neutrophils as a result of RP‐3 treatment (RP‐3 group). A kinetic study showed that the serum transaminase titer of the RP‐3 group was significantly lower than that of the positive control group from 4 to 24 h after LPS injection. The transaminase level was significantly lower in the group with less than 400/mm3 peripheral blood neutrophils than in the group with a greater number. The effect of RP‐3 on the transaminase level was due neither to the injection of cancer ascites nor to RP‐3 injection with the accompanying decrease in complement titer. These results suggest that neutrophils play an important role in the induction of liver dysfunction in this system.