The production of three cytokines, interferon gamma (IFN-y), interleukin 10 (1L-10) and interleukin 12 (IL-12), was measured after intraperitoneal infection of immunocompetent Balb/c mice and immunodeficient SCID mice with the microsporidian, Encephalitozoon cuniculi Levaditi, Nicolau ct Schoen, 1923. High levels of IFN-y were detected in ex vivo cultures of peritoneal exudate cells (PEC) of Balb/c mice, a lower, but earlier IFN-y response was observed in PEC from SCID mice. The early 1L-10 response was detected in ex vivo cultures of splenocytes from Balb/c but not from SCID mice, explaining a delay in the IFN-y response in Balb/c mice. IL-12 was detected in PEC cultures from SCID mice, indicating an alternative pathway of IFN-y production by NK. cells stimulated by IL-12 derived from macrophages.
An experimental infection with the microsporidian Encephalitozoon cuniculi Levaditi, Nicolau et Schoen, 1923 was studied using a model of immunocompetent BALB/c mice and immunodeficient SCID mice. The course of infection after intraperitoneal inoculation of E. cuniculi spores was evaluated using the presence of spores in peritoneal macrophages as a criterion. First significant decrease in the proportion of infected cells was recorded on day 9 post infection (p.i.) in BALB/c mice. From day 14 p.i. no spores were observed in macrophages from BALB/c mice, while the number of infected macrophages from SCID mice increased until the death of the mice. The natural killer (NK) cell activity of mouse splenocytes was compared with the production of interferon gamma (IFN-γ) by these cells. While in BALB/c mice NK activity peaked on days 9 and 14 p.i., in SCID mice the marked increase of NK activity was recorded close before death of mice, on day 21 p.i. in correlation with the production of IFN-γ. Production of specific antibodies was demonstrated from day 9 p.i. in sera from BALB/c mice. It is concluded that intraperitoneal infection of SCID mice with spores of E. cuniculi results in the marked increase in the number of peritoneal exudate cells and in the percentage of infected cells close before death of mice. Neither high activity of NK cells nor increased production of IFN-γ are sufficient for the recovery of SCID mice from an E. cuniculi infection.