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Encephalitozoon cuniculi Genotype II Concentrates in Inflammation Foci
Journal of Inflammation Research ( IF 4.5 ) Pub Date : 2020-09-25 , DOI: 10.2147/jir.s271628
Klára Brdíčková 1, 2 , Bohumil Sak 3 , Nikola Holubová 3, 4 , Dana Květoňová 3 , Lenka Hlásková 3 , Marta Kicia 5 , Żaneta Kopacz 5 , Martin Kváč 3, 4
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Background: Microsporidia of the genus Encephalitozoon are generally connected with severe infections with lethal outcome in immunodeficient hosts. In immunocompetent hosts, microsporidiosis typically establishes a balanced host–parasite relationship that produces minimal clinically overt disease. Although the alimentary tract represents one of the main primary target tissues, the mechanisms of reaching other tissues during systemic microsporidian infections remain unclear.
Methods: In the present study, we tested the relation between inflammation induction in immunocompetent and immunodeficient mice and the presence of spores of E. cuniculi genotype II in selected organs and in fecal specimens by using molecular and histology methods.
Results: We reported the positive connection between inflammation induction and the significant increase of E. cuniculi genotype II occurrence in inflammation foci in both immunocompetent BALB/c and immunodeficient severe combined immunodeficient (SCID) mice in the acute phase of infection and the re-activation of latent microsporidial infection following inflammation induction in immunocompetent mice.
Conclusion: The results imply possible involvement of immune cells serving as vehicles transporting E. cuniculi genotype II purposefully across the whole host body towards inflammation. With increasing number of records of infections, it is necessary to reconsider microsporidia as agents responsible for various pathologies. The elucidation of possible connection with pro-inflammatory immune responses represents an important challenge with consequences for human health and development of therapeutic strategies.



中文翻译:

穴居脑炎基因型 II 集中在炎症病灶中

背景:脑炎属的微孢子虫通常与严重感染有关,在免疫缺陷宿主中会产生致命的后果。在免疫功能正常的宿主中,微孢子虫病通常会建立一种平衡的宿主-寄生虫关系,从而产生最小的临床明显疾病。尽管消化道是主要的主要靶组织之一,但在全身性微孢子虫感染期间到达其他组织的机制仍不清楚。
方法:在本研究中,我们使用分子和组织学方法测试了免疫功能正常和免疫缺陷小鼠的炎症诱导与选定器官和粪便标本中E. cuniculi基因型 II 孢子的存在之间的关系。
结果:我们报道了炎症诱导与免疫活性 BALB/c 和免疫缺陷严重联合免疫缺陷 (SCID) 小鼠在感染急性期炎症灶中E. cuniculi基因型 II 发生显着增加之间的正相关关系,以及重新激活。免疫活性小鼠炎症诱导后潜伏性微孢子感染的研究。
结论:结果表明免疫细胞可能参与了作为运输E. cuniculi的载体基因型 II 有目的地跨越整个宿主身体朝向炎症。随着感染记录数量的增加,有必要重新考虑微孢子虫作为负责各种病理的代理。阐明与促炎免疫反应的可能联系代表了对人类健康和治疗策略发展产生影响的重要挑战。

更新日期:2020-09-25
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