Abstract
The human blood fluke Schistosoma mansoni causes intestinal schistosomiasis, a widespread neglected tropical disease. Infection of freshwater snails Biomphalaria spp. is an essential step in the transmission of S. mansoni to humans, although the physiological interactions between the parasite and its obligate snail host that determine success or failure are still poorly understood. In the present study, the B. glabrata embryonic (Bge) cell line, a widely used in vitro model for hemocyte-like activity, was used to investigate membrane properties, and assess the impact of larval transformation proteins (LTP) on identified ion channels. Whole-cell patch clamp recordings from Bge cells demonstrated that a Zn2+-sensitive H+ channel serves as the dominant plasma membrane conductance. Moreover, treatment of Bge cells with Zn2+ significantly inhibited an otherwise robust production of reactive oxygen species (ROS), thus implicating H+ channels in the regulation of this immune function. A heat-sensitive component of LTP appears to target H+ channels, enhancing Bge cell H+ current over 2-fold. Both Bge cells and B. glabrata hemocytes express mRNA encoding a hydrogen voltage-gated channel 1 (HVCN1)-like protein, although its function in hemocytes remains to be determined. This study is the first to identify and characterize an H+ channel in non-neuronal cells of freshwater molluscs. Importantly, the involvement of these channels in ROS production and their modulation by LTP suggest that these channels may function in immune defense responses against larval S. mansoni.
Highlights
Schistosomiasis, a neglected tropical disease afflicting over 250 million people worldwide [1], is caused by parasitic flatworms of the genus Schistosoma
Electrical recordings from B. glabrata embryonic (Bge) cells demonstrated the presence of H+ channels that allow hydrogen ions (H+)
Using the whole cell patch clamp technique, we discovered an larval transformation proteins (LTP)-sensitive H+ channel that serves as the dominant ion conductance of Bge cell membranes
Summary
Schistosomiasis, a neglected tropical disease afflicting over 250 million people worldwide [1], is caused by parasitic flatworms of the genus Schistosoma. Schistosoma spp. have a two-host life cycle involving sexual reproduction within a mammalian host and asexual reproduction within a snail intermediate host. Eggs from ruptured intestinal capillaries exit the host by fecal excretion, and upon exposure to freshwater, hatch to release the free-swimming snail-infective miracidia. Miracidia transform through two sporocyst stages, completing their life cycle by the production and release of free-swimming cercariae, the human-infective stage [4]. Because of the absolute dependency of human schistosome transmission on the snail host, one of the keys to sustained control of schistosomiasis is to block or eliminate the snail’s participation in the life cycle
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