Authors
E A Pila1; M A Gordy2; V K Phillips2; A L Kabore1; S P Rudko1; P C Hanington1; 1 Univeristy of Alberta, Canada; 2 University of Alberta, Canada Discussion
The digenean trematode Schistosoma mansoni is one of the causative agents of human schistosomiasis, a chronic and devastating disease that affects over 260 million people worldwide. To complete their life cycle, schistosomes must undergo their larval development within specific species of snail intermediate hosts. The specificity in host requirement presents an opportunity for utilizing the snail as a possible target for schistosomiasis control efforts. Compatibility between the snail host and S. mansoni is determined in part by the snail immune response, mediated primarily by the haemocytes as well as soluble immune factors. However, very little is known about endogenous control of haemocyte development in any gastropod model. Here, we present the functional report of a snail endogenous growth factor, granulin (BgGRN). This granulin was identified as part of a peptide screen of snail plasma proteins that differed in abundance between the S. mansoni-resistant (BS-90) and susceptible (M-line) strains of Biomphalaria glabrata. BgGRN transcript expression was found to be responsive in both BS-90 and M-line snails when challenged with S. mansoni increasing 39 and 16 folds respectively relative to β-actin (non-immune control gene). Injection of recombinant BgGRN induced haemocyte proliferation in the snails, particularly of the adherent haemocyte subset that is known to participate in the anti-digenean response. BgGRN-induced proliferation of this haemocyte subset in M-line snails prior to parasite challenge resulted in significant reversal of the highly susceptible phenotype, yielding a 54 % reduction ininfection success. This represents the first functional characterization of an endogenous growth factor of any gastropod mollusc, and is also the first gain-of-resistance study in a snail-digenean infection model using a defined factor to induce snail resistance to infection. 
