Characterization of a Murine Model for <i>Encephalitozoon hellem</i> Infection after Dexamethasone Immunosuppression
Background: <i>Encephalitozoon hellem</i> (<i>E. hellem</i>) belongs to a group of opportunistic pathogens called microsporidia. Microsporidia infection symptoms vary and include diarrhea, ocular disorders and systemic inflammations. Traditionally, immunodeficient animals wer...
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2020-11-01
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author | Guozhen An Yunlin Tang Biying Mo Maoshuang Ran Xiao He Jialing Bao Zeyang Zhou |
author_facet | Guozhen An Yunlin Tang Biying Mo Maoshuang Ran Xiao He Jialing Bao Zeyang Zhou |
author_sort | Guozhen An |
collection | DOAJ |
description | Background: <i>Encephalitozoon hellem</i> (<i>E. hellem</i>) 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 <i>E. hellem</i> infection. Methods: Wild-type C57BL/6 mice were immunosuppressed with dexamethasone (Dex) and then <i>E. hellem</i> 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 <i>E. hellem</i> inoculation resulted in a disseminated nonlethal infection. Interestingly, <i>E. hellem</i> infection desensitized the innate immunity of the host, as shown by cytokine expressions and dendritic cell maturation. We also found that <i>E. hellem</i> 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. |
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spelling | doaj.art-870987ab0bf54b4795115bcd10b940bd2023-11-20T22:53:01ZengMDPI AGMicroorganisms2076-26072020-11-01812189110.3390/microorganisms8121891Characterization of a Murine Model for <i>Encephalitozoon hellem</i> Infection after Dexamethasone ImmunosuppressionGuozhen An0Yunlin Tang1Biying Mo2Maoshuang Ran3Xiao He4Jialing Bao5Zeyang Zhou6State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, ChinaState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, ChinaState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, ChinaState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, ChinaCollege of Sericulture, Textile and Biomass Sciences, Southwest University, Chongqing 400715, ChinaState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, ChinaState Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, ChinaBackground: <i>Encephalitozoon hellem</i> (<i>E. hellem</i>) 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 <i>E. hellem</i> infection. Methods: Wild-type C57BL/6 mice were immunosuppressed with dexamethasone (Dex) and then <i>E. hellem</i> 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 <i>E. hellem</i> inoculation resulted in a disseminated nonlethal infection. Interestingly, <i>E. hellem</i> infection desensitized the innate immunity of the host, as shown by cytokine expressions and dendritic cell maturation. We also found that <i>E. hellem</i> 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.https://www.mdpi.com/2076-2607/8/12/1891microsporidia<i>Encephalitozoon hellem</i>dexamethasonemurine modelimmunity |
spellingShingle | Guozhen An Yunlin Tang Biying Mo Maoshuang Ran Xiao He Jialing Bao Zeyang Zhou Characterization of a Murine Model for <i>Encephalitozoon hellem</i> Infection after Dexamethasone Immunosuppression Microorganisms microsporidia <i>Encephalitozoon hellem</i> dexamethasone murine model immunity |
title | Characterization of a Murine Model for <i>Encephalitozoon hellem</i> Infection after Dexamethasone Immunosuppression |
title_full | Characterization of a Murine Model for <i>Encephalitozoon hellem</i> Infection after Dexamethasone Immunosuppression |
title_fullStr | Characterization of a Murine Model for <i>Encephalitozoon hellem</i> Infection after Dexamethasone Immunosuppression |
title_full_unstemmed | Characterization of a Murine Model for <i>Encephalitozoon hellem</i> Infection after Dexamethasone Immunosuppression |
title_short | Characterization of a Murine Model for <i>Encephalitozoon hellem</i> Infection after Dexamethasone Immunosuppression |
title_sort | characterization of a murine model for i encephalitozoon hellem i infection after dexamethasone immunosuppression |
topic | microsporidia <i>Encephalitozoon hellem</i> dexamethasone murine model immunity |
url | https://www.mdpi.com/2076-2607/8/12/1891 |
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