An Guozhen, Tang Yunlin, Mo Biying, Ran Maoshuang, He Xiao, Bao Jialing, Zhou Zeyang
State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, China.
Chongqing Key Laboratory of Microsporidia Infection and Control, Southwest University, Chongqing 400715, China.
Microorganisms. 2020 Nov 29;8(12):1891. doi: 10.3390/microorganisms8121891.
() 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 infection.
Wild-type C57BL/6 mice were immunosuppressed with dexamethasone (Dex) and then 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.
Histopathological analysis demonstrated that inoculation resulted in a disseminated nonlethal infection. Interestingly, infection desensitized the innate immunity of the host, as shown by cytokine expressions and dendritic cell maturation. We also found that infection greatly altered the composition of host gut microbiota. (4) Conclusions: Dex-immunosuppressed mice provide a useful tool for study microsporidiosis and the interactions between microsporidia and host immunity.
（）属于一类被称为微孢子虫的机会性病原体。微孢子虫感染症状各异，包括腹泻、眼部疾病和全身性炎症。传统上，免疫缺陷动物被用于研究微孢子虫感染。为了克服使用免疫缺陷小鼠进行饲养和操作的困难，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理学免疫抑制的小鼠感染模型。
野生型C57BL/6小鼠用 dexamethasone（地塞米松，Dex）进行免疫抑制，然后将（）孢子经腹腔接种到小鼠体内。对照组为接受Dex免疫抑制但未接种的小鼠，以及接受Dex免疫抑制后再用脂多糖（LPS）处理的小鼠。监测小鼠体重，并在接种后第15天处死所有动物。收集并处理组织碎片和免疫细胞。
组织病理学分析表明，（）接种导致了播散性非致死性感染。有趣的是，如细胞因子表达和树突状细胞成熟所示，（）感染使宿主的先天免疫脱敏。我们还发现，（）感染极大地改变了宿主肠道微生物群的组成。（4）结论：Dex免疫抑制小鼠为研究微孢子虫病以及微孢子虫与宿主免疫之间的相互作用提供了一个有用的工具。
