BAYNE, CJ; BENDER, RC; BRODERICK, EJ; GOODALL, CP; Oregon State University; Oregon State University; Oregon State University; Oregon State University: A genetic basis for resistance to Schistosoma mansoni in Biomphalaria glabrata.
Parasites normally elicit different degrees of pathology among members of a host population, due in part to host genetic polymorphisms. In the Schistosoma mansoni-Biomphalaria glabrata parasitism, susceptibility and resistance to schistosomes are heritable traits. The respiratory burst and its products (reactive oxygen and nitrogen species) are central to the immune defense of the snails. We postulated that the genetic basis for the susceptibility-resistance dichotomy resides in genes encoding enzymes involved in the respiratory burst of the snail hemocyte. We now report that, consistent with this hypothesis, hemocytes from snails that are resistant to the PR1 strain of S. mansoni have a higher capacity to produce hydrogen peroxide (H2O2) than hemocytes from schistosome-susceptible snails. Furthermore, activity of superoxide dismutase (SOD, an enzyme that catalyzes rapid conversion of superoxide anions to H2O2) is higher in hemocytes of resistant snails, and such hemocytes contain twice as much mRNA for cytoplasmic Cu/Zn SOD (SOD1). Among 5 strains of B. glabrata that we have examined, 3 that are resistant to PR1 strain S. mansoni are different from the 2 susceptible strains at the genomic level for the gene encoding SOD1. While mechanisms other than the respiratory burst may influence outcomes, our research suggests that the capacity to generate reactive oxygen species is a major determinant of parasite fates in this host-parasite system. Supported by AI-16137.
