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Published on: November 12, 2015
Host gastric corpus microenvironment facilitates Ascaris suum larval hatching and infection in a murine model
Yifan Wu1, Grace Adeniyi-Ipadeola2, Mahliyah Adkins-Threats3,4,5
1Department of Pediatrics, Division of Pediatric Tropical Medicine, Baylor College of Medicine, Houston, Texas, United States of America.
Insights
Ascariasis roundworm larvae hatch in the stomach, not the small intestine, using acidic mammalian chitinase (AMCase). Targeting AMCase and stomach acid reduces parasitic infection and lung disease.
Area of Science:
- Parasitology
- Gastroenterology
- Immunology
Background:
- Ascariasis is a prevalent global helminth infection, primarily affecting children and causing significant morbidity, including chronic lung disease.
- Infection occurs through oral ingestion of Ascaris eggs, with the traditional understanding being that hatching and larval migration initiate in the small intestine.
Purpose of the Study:
- To investigate the precise location and mechanism of Ascaris egg hatching in the host.
- To identify potential therapeutic targets for preventing ascariasis and associated diseases.
Main Methods:
- Utilized a murine model to study Ascaris suum infection.
- Analyzed larval hatching in the gastric environment.
- Investigated the role of acidic mammalian chitinase (AMCase) and gastric acid.
- Assessed the impact of antagonizing AMCase and gastric acid on parasitic burden and lung disease.
Main Results:
- Demonstrated that Ascaris suum larvae hatch in the host stomach, specifically on the gastric epithelium.
- Showed that larvae require AMCase from chief cells and gastric acid from parietal cells for egg hatching.
- Found that inhibiting AMCase and gastric acid significantly reduced parasitic burden in the liver and lungs and attenuated lung disease.
Conclusions:
- The gastric corpus is the primary site for Ascaris egg hatching, challenging previous assumptions.
- AMCase plays a critical role in the initial stage of ascariasis.
- Targeting AMCase and gastric acid presents a novel therapeutic strategy for ascariasis and related pathologies.
Abstract:
Ascariasis (roundworm) is the most common parasitic helminth infection globally and can lead to significant morbidity in children including chronic lung disease. Children become infected with Ascaris spp. via oral ingestion of eggs. It has long been assumed that Ascaris egg hatching and larval translocation across the gastrointestinal mucosa to initiate infection occurs in the small intestine. Here, we show that A. suum larvae 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. Given Ascaris eggs 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.
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