ArticleInfection and immunity2002
Penicillium marneffei causes osteopontin-mediated production of interleukin-12 by peripheral blood mononuclear cells.
Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 42 citations in OpenAlex.
- Effects ofToxics · 2023Article
- Both Full-Length and Protease-Cleaved Products of Osteopontin Are Elevated in Infectious Diseases.Biomedicines · 2021Review
- The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors.Frontiers in immunology · 2018Review
- Osteopontin ablation ameliorates muscular dystrophy by shifting macrophages to a pro-regenerative phenotype.The Journal of cell biology · 2016Article
- Elevated OPN, IP-10, and neutrophilia in loop-mediated isothermal amplification confirmed tuberculosis patients.Mediators of inflammation · 2014Article
- Danger signals in the initiation of the inflammatory response after myocardial infarction.Mediators of inflammation · 2013Review
- The role of osteopontin (OPN/SPP1) haplotypes in the susceptibility to Crohn's disease.PloS one · 2011Article
- Penicillium marneffei infection and recent advances in the epidemiology and molecular biology aspects.Clinical microbiology reviews · 2006Review
- T-bet-dependent expression of osteopontin contributes to T cell polarization.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the role of osteopontin (OPN) in interleukin-12 (IL-12) production from peripheral blood mononuclear cells (PBMCs) stimulated with Penicillium marneffei. Kinetic studies showed that OPN synthesis preceded that of IL-12 at both mRNA and protein levels when PBMCs were cocultured with P. marneffei. Treatment with anti-OPN monoclonal antibodies (MAb) significantly suppressed IL-12 secretion. Furthermore, native OPN induced a profound level of synthesis of IL-12 from noninfected PBMCs. The major cellular source of OPN was monocytes, because depletion of CD14(+) cells resulted in the abrogation of such production. We also examined the regulatory role of granulocyte-macrophage colony-stimulating factor (GM-CSF) in OPN secretion from P. marneffei-stimulated PBMCs. Neutralizing anti-GM-CSF MAb significantly reduced OPN secretion, and treatment with this cytokine induced OPN production from both infected and noninfected PBMCs. Finally, antagonists against the mannose receptor but not the beta-glucan receptor almost completely abrogated the production of OPN. Our results demonstrated that OPN secreted from monocytes is involved in the production of IL-12 from PBMCs after stimulation with P. marneffei and that OPN production is regulated by GM-CSF. Our results also indicated the possible involvement of the mannose receptor as a signal-transducing receptor for triggering the secretion of OPN by P. marneffei-stimulated PBMCs.
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