Abstract
The 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. Thus, 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. The animals were euthanized with 50 (acute infection) and 120 (chronic infection) days of infection. All infected animals exhibited liver inflammation. Intense granulomatous inflammation 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 inflammation in coinfected animals was characterized by intense neutrophils accumulation and reduced eosinophils number. IFN-γ, IL-2, IL-4, and IL-5 circulating levels were increased in all infected groups. Coinfected animals presented attenuated IFN-γ and IL-4 production in the acute and chronic infections. Taken together, our findings indicate that coinfected animals exhibited a differential modulation of granulomatous inflammation during the acute and chronic phases of infection, which was potentially associated with a divergent profile of cytokines production and migration of neutrophils and eosinophils in response to S. mansoni and P. brasiliensis antigenic stimulation.
Highlights
The development of infectious diseases is deeply influenced by the interaction between pathogen phenotype and host conditions, such as immunological health and presence of comorbidities, including coinfections [1,2,3]
It is possible that P. brasiliensis infection change the granulomatous inflammation and organ damage in Schistosoma-infected hosts. Considering these hypothesis, by using an experiment model of S. mansoni and P. brasiliensis coinfection, we investigated if these infections might interact to change cytokines production and organ damage in mice
In acute the phase of infection, S. mansoni eggs and schistosomiasis granulomas were clearly observed in liver tissue of both infected groups
Summary
The development of infectious diseases is deeply influenced by the interaction between pathogen phenotype (i.e., infectivity, pathogenicity, and virulence) and host conditions, such as immunological health and presence of comorbidities, including coinfections [1,2,3]. Coinfections are typically determined by pathogens that share common endemic areas [9], such Schistosoma mansoni that causes schistosomiasis in Latin America [10] and the fungus Paracoccidioides brasiliensis, the etiological agent of paracoccidioidomycosis [11]. Schistosomiasis is a neglected parasitic disease responsible for more than 230 million people infected in more than 74 countries [10, 12]. P. brasiliensis infects about 10 million people in Latin America [13, 14] After infection with this thermodimorphic fungus, body temperature of the infected host contributes to transform infective forms (i.e., conidia or mycelial fragments) into its pathogenic forms (yeast-like), which may determine clinical manifestations ranging from asymptomatic infection to severe and disseminated disease [11, 15, 16]. Schistosoma mansoni and P. brasiliensis share common endemic areas [4, 18], coinfections with these pathogens remains overlooked
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