ArticlePLoS neglected tropical diseases2016
Osteopontin Is Upregulated in Human and Murine Acute Schistosomiasis Mansoni.
Article in PLoS neglected tropical diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- Single-Cell Analysis Reveals the Cellular and Molecular Changes of Liver Injury and Fibrosis in Mice During the Progression ofCurrent issues in molecular biology · 2024Article
- Dynamics of osteopontin levels and correlation with parasitemia in acute malaria in Uganda and Sweden.BMC infectious diseases · 2024Article
- Osteopontin and malaria: no direct effect on parasite growth, but correlation with P. falciparum-specific B cells and BAFF in a malaria endemic area.BMC microbiology · 2021Article
- Both Full-Length and Protease-Cleaved Products of Osteopontin Are Elevated in Infectious Diseases.Biomedicines · 2021Review
- Praziquantel Treatment ofFrontiers in immunology · 2021Article
- Infection with Hepatitis B Virus May Increase the Serum Concentrations of Osteopontin.Intervirology · 2021Article
- Host Regulators of Liver Fibrosis During Human Schistosomiasis.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
14 authors at 8 institutions in 4 countries.
Funding
Abstract
backgroundSymptomatic acute schistosomiasis mansoni is a systemic hypersensitivity reaction against the migrating schistosomula and mature eggs after a primary infection. The mechanisms involved in the pathogenesis of acute schistosomiasis are not fully elucidated. Osteopontin has been implicated in granulomatous reactions and in acute hepatic injury. Our aims were to evaluate if osteopontin plays a role in acute Schistosoma mansoni infection in both human and experimentally infected mice and if circulating OPN levels could be a novel biomarker of this infection. METHODOLOGY/PRINCIPAL
findingsSerum/plasma osteopontin levels were measured by ELISA in patients with acute (n = 28), hepatointestinal (n = 26), hepatosplenic (n = 39) schistosomiasis and in uninfected controls (n = 21). Liver osteopontin was assessed by immunohistochemistry in needle biopsies of 5 patients. Sera and hepatic osteopontin were quantified in the murine model of schistosomiasis mansoni during acute (7 and 8 weeks post infection, n = 10) and chronic (30 weeks post infection, n = 8) phase. Circulating osteopontin levels are increased in patients with acute schistosomiasis (p = 0.0001). The highest levels of OPN were observed during the peak of clinical symptoms (7-11 weeks post infection), returning to baseline level once the granulomas were modulated (>12 weeks post infection). The plasma levels in acute schistosomiasis were even higher than in hepatosplenic patients. The murine model mirrored the human disease. Macrophages were the major source of OPN in human and murine acute schistosomiasis, while the ductular reaction maintains OPN production in hepatosplenic disease. Soluble egg antigens from S. mansoni induced OPN expression in primary human kupffer cells. CONCLUSIONS/SIGNIFICANCE: S. mansoni egg antigens induce the production of OPN by macrophages in the necrotic-exudative granulomas characteristic of acute schistosomiasis mansoni. Circulating OPN levels are upregulated in human and murine acute schistosomiasis and could be a non-invasive biomarker of this form of disease.
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