Abstract
The capacity of rat peritoneal neutrophils to adhere to and kill schistosomula of S. mansoni in vitro was investigated. Neutrophils adhere readily to schistosomula in the presence of antibody plus complement (C) (fresh immune rat serum), antibody alone (heat-inactivated immune rat serum) and C alone (fresh normal rat serum) but not with heat-inactivated normal rat serum. Schistosomular killing is only achieved with neutrophils and fIRS or fNRS. In the presence of hiIRS the cells detach after 6 h without producing a significant level of parasite death. The system involving neutrophils plus fIRS is the most efficient in terms of serum dilution and the rate of schistosomular killing. The complement-dependent antibody involved in this system belongs to the class IgG and occurs in rat serum at peak titers, 6-8 wk after a primary schistosome infection. Neutrophil adherence in the presence of fNRS depends upon the generation of C3b [fraction b of complement component 3] molecules at the parasite surface via the alternative pathway of C activation. Studies on the antibody alone system indicate that the lack of significant schistosomular killing might result from the absence of factors which stimulated cell migration, since if a chemokinetic agent is introduced into the assay a 30% increase in mortality is recorded. The possible participation of neutrophils in the destruction of a primary and/or challenge infection in vivo is discussed.