RECOMBINANT HUMAN INTERLEUKIN-1-MEDIATED KILLING OF SCHISTOSOMA-MANSONI PRIMARY SPOROCYSTS IN BIOMPHALARIA-GLABRATA

Previous work has indicated that injection of recombinant-human interl eukin (rhIL)-1 beta in Schistosoma mansoni-infected M-line Biomphalari a glabrata resulted in a significant reduction in the number of cercar iae shed. The purpose of the present work was to determine if primary sporocysts were killed following rhIL-1 beta-injection in susceptible snails and, if so, to determine if killing was the direct result of he mocyte activity. Counting of primary sporocysts indicated a 50% reduct ion in the number surviving at 3 days PE in snails from 2 susceptible strains following injection. Histological analysis indicated that kill ing occurred with little-to-no observable hemocyte/parasite contact, w hereas short-term culture of primary sporocysts with cell-free plasma (hemolymph) from injected snails rapidly initiated killing in vitro. B ecause levels of a snail IL-l-like molecule (SnaIL-1) drop significant ly following schistosome exposure in M-line snails, because resistant snails maintain higher SnaIL-1 levels following infection, and because rhIL-1 beta upregulates hemocyte cytotoxic mechanisms, these data sup port the contention that SnaIL-1 plays a role in determining resistanc e in B. glabrata. These data also indicate that schistosome death may be separated from parasite encapsulation by hemocytes and that an as y et unidentified humoral killing mechanism/factor may exist in. glabrat a. Lastly, these data further support the hypothesis that cytokine-lik e molecules are important, functionally conserved immunodefense mediat ors in both vertebrates and invertebrates.