AI Article Synopsis
- Schistosomiasis leads to fibrosis and portal hypertension, but why only 4-10% of infected individuals develop a severe form called hepatosplenic schistosomiasis is still unknown.
- In a study of chronically infected male CBA/J mice, 80% developed moderate splenomegaly while 20% exhibited severe hypersplenomegaly, mirroring human cases.
- The study identified osteopontin as a potential biomarker that distinguishes severe disease from mild, suggesting that lack of osteopontin downregulation in chronic phases could contribute to severe fibrosis in patients.
Article Abstract
Schistosomiasis is a major cause of fibrosis and portal hypertension. The reason 4-10% of infected subjects develops hepatosplenic schistosomiasis remains unclear. Chronically infected male CBA/J mice reproduce the dichotomic forms of human schistosomiasis. Most mice (80%) develop moderate splenomegaly syndrome (similar to hepatointestinal disease in humans) and 20% present severe hypersplenomegaly syndrome (analogous to human hepatosplenic disease). We demonstrated that the profibrogenic molecule osteopontin discriminates between mice with severe and mild disease and could be a novel morbidity biomarker in murine and human schistosomiasis. Failure to downregulate osteopontin during the chronic phase may explain why hepatosplenic subjects develop severe fibrosis.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5584370 | PMC |
| http://dx.doi.org/10.1016/j.ijpara.2016.08.004 | DOI Listing |
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