Host Gastric Corpus Microenvironment FacilitatesAscaris SuumLarval Hatching And Infection in a Murine Model

Abstract

AbstractAscariasis (roundworm) is the most common parasitic helminth infection globally and can lead to significant morbidity in children including chronic lung disease. Children become infected withAscarisspp. via oral ingestion of eggs. It has long been assumed thatAscarisegg hatching and larval translocation across the gastrointestinal mucosa to initiate infection occurs in the small intestine. Here, we show thatA. suumlarvae hatched in the host stomach in a murine model. Larvae utilize acidic mammalian chitinase (AMCase; acid chitinase;Chia) from chief cells and acid pumped by parietal cells to emerge from eggs on the surface of gastric epithelium. Furthermore, antagonizing AMCase and gastric acid in the stomach decreases parasitic burden in the liver and lungs and attenuates lung disease. GivenAscariseggs are chitin-coated, the gastric corpus would logically be the most likely organ for egg hatching, though this is the first study directly evincing the essential role of the host gastric corpus microenvironment. These findings point towards potential novel mechanisms for therapeutic targets to prevent ascariasis and identify a new biomedical significance of AMCase in mammals.