Characterization of a Murine Model for Encephalitozoon hellem Infection after Dexamethasone Immunosuppression.

Characterization of a Murine Model for Encephalitozoon hellem Infection after Dexamethasone Immunosuppression.
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地塞米松免疫抑制后脑炎原虫感染小鼠模型的表征

DOI:
10.3390/microorganisms8121891
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发表时间:
2020-11-29
期刊:
影响因子:
4.5
通讯作者:
Zhou Z
Zhou Z
中科院分区:
生物学3区
文献类型:
--
作者:
An G;Tang Y;Mo B;Ran M;He X;Bao J;Zhou Z

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背景:脑孢子虫(E.hellem)属于一组条件致病菌,称为微孢子虫。微孢子虫感染的症状各不相同,包括腹泻、眼部疾病和全身炎症。传统上,免疫缺陷动物被用来研究微孢子虫感染。为了克服免疫缺陷小鼠在维护和操作上的困难,并更好地模拟自然发生的微孢子虫感染,本研究旨在建立一种药物免疫抑制小鼠感染埃希莱姆球虫的模型。方法:用地塞米松(Dex)免疫抑制野生型C57BL/6小鼠,然后将E.Hellem孢子接种于小鼠体内。对照组为地塞米松免疫抑制但未接种的小鼠,地塞米松免疫抑制后的小鼠再经脂多糖(LPS)处理。于接种后第15天监测小鼠体重,处死动物。收集组织碎片和免疫细胞并进行处理。结果:组织病理学分析表明,接种E.hellem可导致播散性非致死性感染。有趣的是,E.hellem感染使宿主的先天免疫减敏,表现为细胞因子的表达和树突状细胞的成熟。我们还发现,E.hellem感染极大地改变了宿主肠道微生物区系的组成。结论:地塞米松免疫抑制小鼠为研究微孢子虫病及其与宿主免疫的相互作用提供了有用的工具。
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.
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