Galván Ana Luz, Agudelo Sonia del Pilar, Restrepo Juan Gonzalo, Toro Fabiola, Galviz Luisa Alejandra, Botero Jorge
Departamento de Microbiología y Parasitología, Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Biomedica. 2006 Mar;26(1):126-37.
Encephalitozoon intestinalis, a parasite belonging to the phylum Microsporidia, is causes gastrointestinal infections in the immunocompromised host. A suitable pharmacologically immunosuppressed animal model for the study of natural E. intestinalis infection, which can establish the immune components that respond to this parasite, is lacking.
To evaluate the effect of immunosuuppression with Cyclosporine A (CsA) in C57BL/ 6 mice on experimental infection with E. intestinalis infection.
Eighty C57BL/6 mice were distributed in four treatment groups: Control, CsA-immunosuppressed mice without infection, immunocompetent and immunossuppressed mice infected with E. intestinalis. Mice were immunosuppressed with a weekly dose of 50 mg/Kg body weight of CsA, during the course of the study. Five mice from each group were sacrificed 2, 3, 4 and 6 weeks post-infection, to obtain blood for antibody testing and stool samples were analyzed to assess excretion of spores.
Production of specific IgG antibodies was significantly higher in the immunocompetent group as compared to the immunosuppressed group of experimentally infected mice. In the infected mice, parasites were not observed in any tissues different from the small intestine. However, spore excretion through the stool and duodenal liquid was higher in the group of immunosuppresed infected mice.
Immunosuppression induced with CsA in the murine model did not allow parasite dissemination and illness progression, but raised kinetics of spore excretion and decreased the production of IgG antibodies.