Investigating host immune responses to Schistosoma mansoni cercaria in acute schistosomiasis 4192

Abstract Description Schistosomiasis is a prevalent tropical parasitic disease caused, in part, by the helminthic parasite Schistosoma mansoni (S. mansoni) affecting more than 200 million people globally. Some patients house chronic infection with minimal symptomology; however, 5-10% present with severe immunopathology. In the context of established infection, eggs are highly inflammatory and result in hepatic granulomas, whereas adult worms are immunosuppressive and allow parasitic survival in the host if left untreated. Currently, there is no consensus as to whether the cercaria are inflammatory or immunosuppressive during invasion. Cercaria are the only life stage that is infectious to mammalian hosts. Thus, this stage has the potential for therapeutic implications by which disease severity can be reduced. Previous studies have attempted to dissect the role cercaria and schistosomula in host immune response to parasitic invasion. Along with determining robust methods for maintaining viable cercaria, we hypothesized that presenting cercarial components dictate the host immune response. We found that the insoluble cercarial material most strongly elicits a pro-inflammatory response mediated by C-type lectin receptor Dectin-1 in macrophages. Additionally, it was determined that inflammasome related genes are upregulated in response to cercarial components. Together, we conclude cercaria elicit proinflammatory responses from the host via Dectin-1 mediated inflammasome priming and activation. Funding Sources Supported by NIH/NIAID R01 AI148656; NIH/NIGMS T32GM108563-06 and T32GM154124-01. Topic Categories Microbial, Parasitic, and Fungal Immunology (MPF)