Can immunosuppressed mice control oral infection by the opportunistic pathogenEncephalitozoon intestinalis?

Abstract

Intestinal mucosa (IM), or the outer surface of the intestine, serves at the primary site for the interaction of various pathogens that cause infection via the oral route. Thus, IM is crucial for developing an efficient adaptive immune response against pathogenic micro-organisms, thereby preventing their colonization and subsequent infection. In the present study, we investigated the immune response to Encephalitozoon intestinalis-caused infection in the IM and gut-associated lymphoid tissue (GALT) in C57BL/6 female mice. To mimic an immunosuppressive condition, the mice were treated with cyclophosphamide (Cy). Histopathology revealed lymphoplasmacytic enteritis at 7 and 14 days-post-infection (dpi) in all infected groups; however, inflammation diminished at 21 and 28 dpi. Cy treatment also led to a higher number of E. intestinalis spores and lesions, which reduced at 28 dpi. In addition, flow cytometry analysis demonstrated CD4+ and CD8+ T cells to be predominant immune cells, with a significant increase in both Th1 and Th2 cytokines at 7 and 14 dpi, as demonstrated by histopathology. In conclusion, Cy treatment reduced GALT (Peyer’s plaques and mesenteric lymph nodes) and peritoneum populations but increased the T-cell population in the intestinal mucosa and the production of pro-inflammatory cytokines, which were able to eliminate this opportunistic fungus and reduced the infection.