Trypanosoma cruzi Y株再感染マウスの腸管免疫病理学的評価

Chagas disease, caused by the protozoan Trypanosoma cruzi, is influenced by both host-related factors and parasite characteristics, including reinfection and strain variability. While the heart is the primary focus of reinfection studies, the effects on the intestinal form of the disease remain poorly understood.

In this study, C57BL/6 male mice were infected and subsequently reinfected with the T. cruzi Y strain to assess the immunopathological consequences in the intestinal tract. We analyzed parasitemia levels, systemic cytokines, anti-T. cruzi immunoglobulin levels (IgG, IgG2a, IgG2b), inflammatory infiltrates, neuronal counts, and collagen deposition. Our data showed that reinfection led to reduced parasitemia and did not alter antibody levels generated during primary infection. However, reinfection induced a systemic reduction in IL-4 and IL-10 and an increase in IFN-γ, indicating a shift toward a pro-inflammatory profile. Histopathologically, reinfected mice exhibited intensified intestinal inflammation and increased neuronal destruction in the myenteric plexus, without additional collagen deposition compared to singly infected animals.

Although homologous reinfection may enhance parasitemia control through sustained immunoglobulin responses, it exacerbates tissue inflammation and neuronal damage. These findings underscore the dual role of immune responses in controlling parasite burden while potentially contributing to intestinal pathology, highlighting the need for caution when considering reinfection risks in endemic areas.