Apoptosis in the intestines of mice infected with Acanthamoeba sp.

Introduction: Acanthamoeba spp. are parasites that typically colonize the brain, cornea, and lungs. However, some studies suggest that amoebas may also be present in the gut microbiome, as they have been found in the stool of healthy humans and animals. Given research indicating that parasites in the small and/or large intestine may modulate apoptosis, this study aimed to assess apoptosis in the small intestines of mice infected with Acanthamoeba sp. Materials and methods: The small intestines used in this study were collected from immunocompetent and immunosuppressed mice experimentally infected with Acanthamoeba sp. (AM22 strain, GenBank reference number: GQ342607). The intestines were homogenized, and the expression of pro-apoptotic Bax, anti-apoptotic Bcl-2, caspase 9 (Cas9) and caspase 3 (Cas3) proteins was determined using the Western blot method. The results were statistically analyzed.Results: In immunocompetent mice infected with Acanthamoeba sp., there was an increase in the protein expression of the pro-apoptotic Bax. The level of the anti-apoptotic protein Bcl-2 was higher at each time point compared to the group of uninfected animals. The Bax/Bcl-2 ratio was similar in immunocompetent infected and uninfected mice, with no statistically significant difference. The levels of Cas9 and Cas3 in immunocompetent infected and uninfected mice were also similar. In immunosuppressed mice, increased Bax expression was found on days 16 and 24 post Acanthamoeba sp. infection. On the same days, a reduced level of Bcl-2 and statistically significant differences in the Bax/Bcl-2 ratio were observed compared to mice in the control group. Increased expressions of Cas9 and Cas3 were also observed at 16 and 24 days post-inoculation (dpi).Conclusions: In immunocompetent hosts, systemic acanthamoebiasis does not affect every organ. However, infection with Acanthamoeba spp. in immunosuppressed hosts induces the apoptosis pathway in intestinal epithelial cells.