Abstract
During its life cycle, the helminth parasite Schistosoma mansoni uses the freshwater snail Biomphalaria glabrata as an intermediate host to reproduce asexually generating cercariae for infection of the human definitive host. Following invasion of the snail, the parasite develops from a miracidium to a mother sporocyst and releases excretory-secretory products (ESPs) that likely influence the outcome of host infection. To better understand molecular interactions between these ESPs and the host snail defence system, we determined gene expression profiles of haemocytes from S. mansoni-resistant or -susceptible strains of B. glabrata exposed in vitro to S. mansoni ESPs (20 μg/ml) for 1 h, using a 5K B. glabrata cDNA microarray. Ninety-eight genes were found differentially expressed between haemocytes from the two snail strains, 57 resistant specific and 41 susceptible specific, 60 of which had no known homologue in GenBank. Known differentially expressed resistant-snail genes included the nuclear factor kappa B subunit Relish, elongation factor 1α, 40S ribosomal protein S9, and matrilin; known susceptible-snail specific genes included cathepsins D and L, and theromacin. Comparative analysis with other gene expression studies revealed 38 of the 98 identified genes to be uniquely differentially expressed in haemocytes in the presence of ESPs, thus identifying for the first time schistosome ESPs as important molecules that influence global snail host-defence cell gene expression profiles. Such immunomodulation may benefit the schistosome, enabling its survival and successful development in the snail host.
Highlights
The parasite Schistosoma mansoni causes the neglected tropical disease human intestinal schistosomiasis, and has a complex life cycle that involves a freshwater snail intermediate host, a human definitive host, and free-living motile stages that enable movement between hosts [1]
We have recently shown that S. mansoni excretory-secretory products (ESPs) suppress signalling by extracellular signal-regulated kinase (ERK) in haemocytes from S. mansoni-susceptible B. glabrata [18] and that such suppression likely affects heat shock protein 70 (HSP70) [19] and nitric oxide (NO) [16] levels in a dose dependent fashion
Expression Profiling by Microarray The 5K microarray was used here to compare directly gene expression in haemocytes derived from schistosome-resistant and susceptible B. glabrata when treated with S. mansoni ESPs produced during miracidia to mother sporocyst development
Summary
The parasite Schistosoma mansoni causes the neglected tropical disease human intestinal schistosomiasis, and has a complex life cycle that involves a freshwater snail intermediate host, a human definitive host, and free-living motile stages that enable movement between hosts [1]. We have recently shown that S. mansoni ESPs suppress signalling by extracellular signal-regulated kinase (ERK) in haemocytes from S. mansoni-susceptible B. glabrata [18] and that such suppression likely affects HSP70 [19] and NO [16] levels in a dose dependent fashion. This supports the interference theory [20] (reviewed by [21]) whereby the parasite is able to suppress the host response to enable it to establish an infection. The extent to which ESPs modulate global gene expression of haemocytes remains an important and unanswered question
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
