SCHISTOSOMA-MANSONI - INTERLEUKIN-1 INCREASES PHAGOCYTOSIS AND SUPEROXIDE PRODUCTION BY HEMOCYTES AND DECREASES OUTPUT OF CERCARIAE IN SCHISTOSOME-SUSCEPTIBLE BIOMPHALARIA-GLABRATA

Decreases in the number of Schistosoma mansoni cercariae released from susceptible M-line Biomphalaria glabrata were detected following inje ction with the recombinant human cytokine, interleukin-1. No differenc es in either the time postexposure at which shedding began or the perc entage of snails shedding cercariae were detected between interleukin- 1 injected, heat-inactivated interleukin-1 injected, or sham injected controls. However, sham injected and heat-inactivated interleukin-1 in jected snails maintained significantly higher (approximately three-fol d) levels of cercarial production compared to interleukin-l injected s nails over 8 weeks of cercarial shedding. Injection of interleukin-l i nto schistosome-susceptible (M-line) and resistant (13-16-R1) strains of B. glabrata increased hemocyte phagocytosis of target particles and phagocytosis stimulated O-2(-) production in both snail strains at 24 hr postexposure to the parasite. Resistant 13-16-R1 snails maintained , on average, 2.4 times the number of O-2(-) producing phagocytic cell s than did M-line susceptible snails, indicating that the incomplete a brogation of cercarial shedding in M-line snails may be due to an inad equate number of activated circulating effector cells in these snails. These data strongly support the contention that the evolutionarily co nserved cytokine, interleukin-l, or a molecule in snail plasma with in terleukin-1-like immunospecificity, biological activity, and function plays a significant role in the maintenance of susceptibility or resis tance to S. mansoni infection in B. glabrata. Finally, these data also supply evidence for the evolutionary conservation of the function and role of interleukin-1, O-2(-) and antioxidant defense mechanisms in t his host-parasite relationship. (C) 1995 Academic Press, Inc.