<p><em>Encephalitozoon cuniculi</em> Genotype II Concentrates in Inflammation Foci</p>

Abstract

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.

Comparison of the Concentration of Encephalitozoon cuniculi Genotypes I and III in Inflammatory Foci Under Experimental Conditions

“…In SCID mice the concentration of microsporidia was the most intense in E. cuniculi genotype III, reaching 1.0×10 7 spores per gram of tissue at 35 DPI, compared to 2.4×10 5 and 5.0×10 5 reported in genotypes I and II, respectively (present study), 48 ( Figure 3A ). This correspond to the data published by Sak et al 55 , 58 , 72 and Kotková et al, 49 , 71 ie, the infection intensity of E. cuniculi genotypes I and II was comparable, whereas E. cuniculi genotype III reached up to two orders higher spore burden.…”

“… 61–63 Recently, a role for the involvement of such immune cells connected with pro-inflammatory immune responses (eg, trafficking macrophages and other phagocytic cells such as neutrophils, monocytes, dendritic cells, and eosinophils) in the expansion of E. cuniculi infection in host tissues has been suggested based on the occurrence of microsporidia in inflamed tissues 47 and the targeted migration seen following experimental induction of inflammation towards inflammation foci. 48 …”

“… 35 , 36 , 44–46 Recently, a possible involvement of immune cells connected with pro-inflammatory immune responses serving as vehicles transporting E. cuniculi genotype II purposefully across the whole host body towards inflammation was suggested, based on the occurrence of microsporidia in inflamed tissues, 47 and experimentally verified. 48 …”

“…The present study was designed to compare the progress of concentration of Encephalitozoon cuniculi genotypes I and III in sites of inflammation with previously published data on E. cuniculi genotype II 48 and to answer the question of whether individual genotypes of E. cuniculi differ in dispersal within the host body following experimentally induced inflammation.…”

Enterocytozoon Bieneusi Infects Children With Inflammatory Bowel Disease Undergoing Immunosuppressive Treatment

“…Furthermore, microsporidia could persist and replicate inside macrophages and in this form, they can be transported throughout the host ( 22 ). Brdíčková et al ( 23 ) have shown that other microsporidial species, E. cuniculi genotype II, migrates to inflammatory foci probably with the contribution of immune cells participating in its formation ( 23 ). If this is the case in patients suffering from chronic inflammatory process, subsequent worsening of the IBD clinical picture might occur.…”