Abstract
Schistosoma mansoni is a parasitic helminth that infects millions of people mostly in tropical parts of the world. Different life cycle stages of S.mansoni, that infect or develop in the human host, promote distinct immune responses and are known for their ability to modulate host immune responses. However, the molecular mechanisms through which the parasites interact with, and modulate the host immune system remain incompletely understood. Despite the well-known ability of various lipids to modulate immune responses, a comprehensive analysis of the lipidome of the different life cycle stages has not been performed. Using three complementary MS-based platforms to detect and quantify around 350 lipid species, we here characterized the lipid profiles of S. mansoni cercariae, worms and eggs, as well as extracts and excretory/secretory (ES) products of different life cycle stages of S. mansoni. We identified life cycle stage specific signatures of lipid classes of which cercariae were found to have the most distinct profile. Moreover, we detected several immunolomodulatory oxylipids in the different life cycle stages. Specifically, prostaglandins were found to be most highly enriched in egg preparations, while resolvins were specifically detected in cercariae. Together, the generation of this detailed lipid database of the different life cycle stages of S. mansoni will not only be important for a better understanding of the biology of the parasite itself but also of host-parasite interactions and how that could result in immunomodulation.
Highlights
Using three lipidomics platforms, which were: QToF based LCMS/MS for major lipid classes, GC-MS for total fatty acid (FA) analysis and QTrap based LC-MS/MS for eicosanoid and docosanoid analysis, we investigated occurrence and quantity of several lipid classes in different life-cycle stages of S. mansoni that could be of relevance to interaction with the human host
In total we identified more than 350 lipid species including several bioactive molecules, which we organized in a S. mansoni lipid database
This specific difference is likely to be a direct result of the fact that because S. mansoni is unable to synthesize fatty acids and sterols de novo [36], it relies on scavenging of lipid precursors from its host to generate complex lipids such as phospholipids and TG [37], a process that free swimming cercariae cannot resort to
Summary
Infection of humans is initiated by the larval stage of these parasites, termed cercariae, through their ability to penetrate human skin. Upon penetration cercariae lose their tail, allowing their head to develop into schistosomula that migrate through the skin into the circulation. A large fraction of the eggs get lodged in the intestinal wall or are instead carried by the blood flow into the liver, where they become trapped in hepatic sinusoids. This accumulation of eggs in tissues is the major cause of pathology in schistosomiasis [2]
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