Taken together, our findings indicate that coinfected animals exhibited a differential modulation of granulomatous inflammation in the acute and chronic phases of infection, which was potentially associated with a divergent profile of cytokines such as IFN-γ, IL-2, IL-4, and IL-5, as well as distinct recruitment of neutrophils and eosinophils in response to S. mansoni and P. brasiliensis antigenic stimulation. Here, IFNG is linked to inflammatory response.