Journal
MEDIATORS OF INFLAMMATION
Volume 2016, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2016/5813794
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Funding
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2007/02487-3, 2007/00840-8, 2011/17611-7]
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [557403/2008-1, 467646/2014-7]
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) [BEX 9320/13-0]
- National Institutes of Health (NIH) [AL101982]
- Nucleo de Apoio a Pesquisa em Doencas Inflamatorias (NAPDIN) [11.1.21625.01.0]
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Histoplasma capsulatum is a dimorphic fungus that develops a yeast-likemorphology in host's tissue, responsible for the pulmonary disease histoplasmosis. The recent increase in the incidence of histoplasmosis in immunocompromised patients highlights the need of understanding immunological controls of fungal infections. Here, we describe our discovery of the role of endogenous galectin-1 (Gal-1) in the immune pathophysiology of experimental histoplasmosis. All infected wild-type (WT) mice survived while only 1/3 of Lgals1(-/-) mice genetically deficient in Gal-1 survived 30 days after infection. Although infected Lgals1(-/-) mice had increased proinflammatory cytokines, nitric oxide (NO), and elevations in neutrophil pulmonary infiltration, they presented higher fungal load in lungs and spleen. Infected lung and infected macrophages from Lgals1(-/-) mice exhibited elevated levels of prostaglandin E-2 (PGE(2), a prostanoid regulator of macrophage activation) and prostaglandin E synthase 2 (Ptgs2) mRNA. Gal-1 did not bind to cell surface of yeast phase of H. capsulatum, in vitro, suggesting that Gal-1 contributed to phagocytes response to infection rather than directly killing the yeast. The data provides the first demonstration of endogenous Gal-1 in the protective immune response against H. capsulatum associated with NO and PGE(2) as an important lipid mediator in the pathogenesis of histoplasmosis.
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