Abstract
Background: Encephalitozoon hellem (E. hellem) belongs to a group of opportunistic pathogens called microsporidia. Microsporidia infection symptoms vary and include diarrhea, ocular disorders and systemic inflammations. Traditionally, immunodeficient animals were used to study microsporidia infection. To overcome the difficulties in maintenance and operation using immunodeficient mice, and to better mimic natural occurring microsporidia infection, this study aims to develop a pharmacologically immunosuppressed murine model of E. hellem infection. Methods: Wild-type C57BL/6 mice were immunosuppressed with dexamethasone (Dex) and then E. hellem spores were inoculated into the mice intraperitoneally. Control groups were the Dex-immunosuppressed but noninoculated mice, and the Dex-immunosuppressed then lipopolysaccharide (LPS)-treated mice. Mice body weights were monitored and all animals were sacrificed at the 15th day after inoculation. Tissue fragments and immune cells were collected and processed. Results: Histopathological analysis demonstrated that E. hellem inoculation resulted in a disseminated nonlethal infection. Interestingly, E. hellem infection desensitized the innate immunity of the host, as shown by cytokine expressions and dendritic cell maturation. We also found that E. hellem infection greatly altered the composition of host gut microbiota. Conclusions: Dex-immunosuppressed mice provide a useful tool for study microsporidiosis and the interactions between microsporidia and host immunity.
Highlights
Microsporidia are a group of intracellular pathogens causing opportunistic infections [1,2]
Most of what is known about the host immune responses against microsporidia are from severe combined immunodeficiency (SCID) or nude animal models, using E. cuniculi or E. intestinalis as infecting pathogens [11,12,13]
Studies showed that cell-mediated immunity, especially the CD8+T lymphocytes mediated cytotoxic effect is important for hosts [14,15,16]
Summary
Microsporidia are a group of intracellular pathogens causing opportunistic infections [1,2]. The infection outcomes and clinical symptoms are associated with pathogen species and hosts immune-state. Most of what is known about the host immune responses against microsporidia are from severe combined immunodeficiency (SCID) or nude animal models, using E. cuniculi or E. intestinalis as infecting pathogens [11,12,13]. To overcome the difficulties in maintenance and operation using immunodeficient mice, and to better mimic natural occurring microsporidia infection, this study aims to develop a pharmacologically immunosuppressed murine model of E. hellem infection. E. hellem infection desensitized the innate immunity of the host, as shown by cytokine expressions and dendritic cell maturation. Conclusions: Dex-immunosuppressed mice provide a useful tool for study microsporidiosis and the interactions between microsporidia and host immunity
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