Research Article Protective Effect of Galectin-1 during Histoplasma capsulatum Infection Is Associated with Prostaglandin E 2 and Nitric Oxide Modulation Lílian Cataldi Rodrigues, 1 Adriana Secatto, 1 Carlos A. Sorgi, 1 Naiara N. Dejani, 2 Alexandra I. Medeiros, 2 Morgana Kelly Borges Prado, 1 Simone Gusmão Ramos, 3 Richard D. Cummings, 4 Sean R. Stowell, 5 Lúcia Helena Faccioli, 1 and Marcelo Dias-Baruffi 1 1 Departamento de An´ alises Cl´ ınicas, Toxicol´ ogicas e Bromatol´ ogicas, Faculdade de Ciˆ encias Farmacˆ euticas de Ribeir˜ ao Preto, Universidade de S˜ ao Paulo (USP), 14040-903 Ribeir˜ ao Preto, SP, Brazil 2 Departamento de Ciˆ encias Biol´ ogicas, Faculdade de Ciˆ encias Farmacˆ euticas, Universidade Estadual Paulista (UNESP), 14801-902 Araraquara, SP, Brazil 3 Departamento de Patologia, Faculdade de Medicina de Ribeir˜ ao Preto, Universidade de S˜ ao Paulo (USP), 14049-900 Ribeir˜ ao Preto, SP, Brazil 4 Department of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115, USA 5 Department of Pathology, Emory University School of Medicine, Atlanta, GA 30322, USA Correspondence should be addressed to Marcelo Dias-Baruf; mdbaruf@fcfrp.usp.br Received 16 April 2016; Revised 27 July 2016; Accepted 1 August 2016 Academic Editor: Marc Pouliot Copyright © 2016 L´ ılian Cataldi Rodrigues et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Histoplasma capsulatum is a dimorphic fungus that develops a yeast-like morphology in host’s tissue, responsible for the pulmonary disease histoplasmosis. Te 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 defcient in Gal-1 survived 30 days afer infection. Although infected Lgals1 −/− mice had increased proinfammatory cytokines, nitric oxide (NO), and elevations in neutrophil pulmonary infltration, 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. Te data provides the frst 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. 1. Introduction Histoplasmosis is a worldwide known disease caused by the fungus Histoplasma capsulatum. Te real geographic distribution of this mycosis could be more widespread than what was previously thought [1, 2]. Te incidence of this fungal disease is higher in the Mid- and Southeast USA, Latin America, China, and other world areas [2]. Addition- ally, asymptomatic cases are escalating and are reported to predominately afect immunocompromised individuals as an acute pulmonary infection similar to mild fu-like symptoms [1, 3, 4]. Likewise, the most severe symptomatic form of the disease, referred to as disseminated histoplasmosis, develops most commonly in immunosuppressed patients. However, unlike the mild form, disseminated histoplasmosis can lead to death [4]. Although antifungal therapies have been used against the fungus, there are no current alternative therapies to treat or protect against H. capsulatum infection. H. capsulatum is a dimorphic, facultative, intracellular pathogen found as a yeast phase when in host tissue [5]. Hindawi Publishing Corporation Mediators of Inflammation Volume 2016, Article ID 5813794, 13 pages http://dx.doi.org/10.1155/2016/5813794