Exacerbation of toxoplasmosis in neutrophil-depleted mice.

Studies were performed to determine whether resistance to Toxoplasma gondii infection in mice depends on a mechanism involving neutrophils. Immunocompetent C57BL/6 and C.B-17 mice infected with T. gondii by gavage had an increased percentage of neutrophils in their peripheral blood. C57BL/6 mice selectively depleted of neutrophils by injections of RB6-8C5 monoclonal antibody died during the acute phase of the disease. Depletion of neutrophils had no effect on interferon gamma production, but had a profound effect on the total numbers of peripheral blood CD4+ and CD8+ T cells. Neutrophil-depleted C.B-17 mice survived longer than neutrophil-depleted C57BL/6 mice when infected with T. gondii, however they became much sicker, and were less able to survive long-term than infected, control mAb-treated mice as indicated by severe sustained weight loss. This study shows that neutrophils play an important role in resistance to acute primary T. gondii infection and that depletion of neutrophils reduces the numbers of CD4+ and CD8+ lymphocytes recoverable from peripheral blood of infected but not uninfected mice. This effect on lymphocytes may contribute to the reduced long-term survival of neutrophil-depleted mice.