Abstract
The outcome of infection in the host snail Biomphalaria glabrata with the digenean parasite Schistosoma mansoni is determined by the initial molecular interplay occurring between them. The mechanisms by which schistosomes evade snail immune recognition to ensure survival are not fully understood, but one possibility is that the snail internal defence system is manipulated by the schistosome enabling the parasite to establish infection. This study provides novel insights into the nature of schistosome resistance and susceptibility in B. glabrata at the transcriptomic level by simultaneously comparing gene expression in haemocytes from parasite-exposed and control groups of both schistosome-resistant and schistosome-susceptible strains, 2 h post exposure to S. mansoni miracidia, using an novel 5K cDNA microarray. Differences in gene expression, including those for immune/stress response, signal transduction and matrix/adhesion genes were identified between the two snail strains and tests for asymmetric distributions of gene function also identified immune-related gene expression in resistant snails, but not in susceptible. Gene set enrichment analysis revealed that genes involved in mitochondrial electron transport, ubiquinone biosynthesis and electron carrier activity were consistently up-regulated in resistant snails but down-regulated in susceptible. This supports the hypothesis that schistosome-resistant snails recognize schistosomes and mount an appropriate defence response, while in schistosome-susceptible snails the parasite suppresses this defence response, early in infection.
Highlights
The tropical freshwater snail Biomphalaria glabrata is an intermediate host for several digenean trematode parasitic worms, including Schistosoma mansoni, the causative agent of human intestinal schistosomiasis
Genes expressed in haemocytes sampled 2 h post exposure to S. mansoni miracidia, were compared to unexposed controls to investigate the initial response of each snail strain to the parasite
The genes differentially expressed between haemocytes of the schistosome-susceptible and schistosome-resistant B. glabrata strains offer great insight into the complex molecular processes that are involved in the defence response to the parasite
Summary
The tropical freshwater snail Biomphalaria glabrata is an intermediate host for several digenean trematode parasitic worms, including Schistosoma mansoni, the causative agent of human intestinal schistosomiasis. The initial interactions between snail and invading schistosome are considered to define their respective future reproduction and survival; the parasite transforming from a short-lived free-living form in freshwater to a longer-term asexual parasitic stage in the snail hosts. The initial molecular interplay between snails and schistosomes is complex and there exists an urgent need to determine the principal pathways controlling this response, since identifying those factors involved in the intricate balance between the snail internal defence system (IDS) and trematode infectivity mechanisms that determine the success or failure of an infection (reviewed in [7,8,9]) may provide insight into approaches to disrupt the parasitic infection in the snail and break transmission. By understanding the basis of compatibility and the mechanisms underlying snail susceptibility to schistosome infection, the levels of compatibility in field situations can be assessed, leading to enhanced understanding of transmission dynamics which could inform control strategies
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