Research Article Impact of Paracoccidioides brasiliensis Coinfection on the Evolution of Schistosoma mansoni-Induced Granulomatous Liver Injury in Mice Matheus Pereira de Araújo, 1 Eva Burger, 1 Rômulo Dias Novaes , 1 Amanda Ami Akatuti, 1 Maria Ângela Rodrigues, 1 Ana Carolina Silvério Cerqueira Mendes, 1 Giulia Maria de Castro Bani, 1 Eliziária Cardoso Santos , 2 Andréia Aparecida Santos Mendonça, 2 and Raquel Lopes Martins Souza 1 1 Instituto de Ciˆ encias Biom´ edicas, Universidade Federal de Alfenas (UNIFAL-MG), Alfenas, Minas Gerais, Brazil 2 School of Medicine, Universidade Federal dos Vales do Jequitionhonha e Mucuri (UFVJM), Diamantina, Minas Gerais, Brazil Correspondence should be addressed to Raquel Lopes Martins Souza; souzaraquel807@gmail.com Received 31 August 2018; Revised 11 February 2019; Accepted 3 March 2019; Published 24 March 2019 Academic Editor: Yujiang Fang Copyright © 2019 Matheus Pereira de Ara´ ujo 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. Te pathogens Schistosoma mansoni and Paracoccidioides brasiliensis share common geographic areas, determining infectious diseases with high mortality rates worldwide. Histopathological and immunological changes induced by each pathogen are well understood; however, the host responses to S. mansoni and P. brasiliensis coinfection are still unknown. Tus, we investigated liver damage and cytokines production in a murine model acutely and chronically coinfected with these pathogens. Fourty male Swiss mice were infected with S. mansoni and P. brasiliensis alone or coinfected. Te animals were euthanized with 50 (acute infection) and 120 (chronic infection) days of infection. All infected animals exhibited liver infammation. Intense granulomatous infammation was detected in animals infected with S. mansoni alone and those coinfected. Productive and involutive granulomas were clearly observed in acute and chronic infections, respectively. Granuloma size was reduced in the acute phase and increased in the chronic phase of S. mansoni and P. brasiliensis coinfection, compared with animals infected only with S. mansoni. In the chronic phase of infection, the granulomatous infammation in coinfected animals was characterized by intense neutrophils accumulation and reduced eosinophils number. IFN-, IL-2, IL-4, and IL-5 circulating levels were increased in all infected groups. Coinfected animals presented attenuated IFN- and IL-4 production in the acute and chronic infections. Taken together, our fndings indicate that coinfected animals exhibited a diferential modulation of granulomatous infammation during the acute and chronic phases of infection, which was potentially associated with a divergent profle of cytokines production and migration of neutrophils and eosinophils in response to S. mansoni and P. brasiliensis antigenic stimulation. 1. Introduction Te development of infectious diseases is deeply infuenced by the interaction between pathogen phenotype (i.e., infec- tivity, pathogenicity, and virulence) and host conditions, such as immunological health and presence of comorbidities, including coinfections [1–3]. Although coinfections are ofen neglected, these diseases are highly prevalent worldwide, especially in developing countries [4, 5]. Coinfections are more dangerous than infections induced by a single pathogen [3, 6], especially considering that divergent (i.e., cellular vs. humoral, or T1 vs. T2 vs. T17) and unbalanced immuno- logical phenotypes simultaneously are required to combat two or more parasite species can compromise the infection resolution [3, 7, 8]. In general, coinfections are typically determined by pathogens that share common endemic areas [9], such Schistosoma mansoni that causes schistosomia- sis in Latin America [10] and the fungus Paracoccidioides brasiliensis, the etiological agent of paracoccidioidomycosis [11]. Hindawi BioMed Research International Volume 2019, Article ID 8319465, 12 pages https://doi.org/10.1155/2019/8319465