Mechanisms of resistance/susceptibility to murine encephalitozoonosis.

Mechanisms of resistance/susceptibility to the obligate intracellular protozoan Encephalitozoon cuniculi were studied in resistant BALB/c and susceptible C57BL/6 mice. Three immunological functions were examined: the production of lymphokine(s) (LK) by T-lymphocytes, the proliferative response of spleen cells to parasite spore fragments, and the ability of splenic and thioglycollate-induced peritoneal macrophages to act as accessory cells in antigen-induced T-cell proliferation. The two strains showed differences in the time required for LK production in vitro but not in their ability to generate LK. Spore fragment-induced lymphoblastogenesis was found in spleen cells of infected BALB/c and C57BL/6 mice. There was no difference between the two strains in dose response and time of maximal response, but the magnitude of maximal response was significantly less in C57BL/6 mice. Indomethacin was found to augment the lymphoproliferative response of C57BL/6 but not BALB/c mice, suggesting that prostaglandin production may be involved in immunosuppression in C57BL/6 mice. C57BL/6 mice required more splenic adherent cells to achieve the same proliferative response as found in BALB/c mice. The ability of thioglycollate-induced peritoneal macrophages to act as accessory cells in antigen-induced T-cell proliferation was less in C57BL/6 mice than in BALB/c mice. Thus, it appeared that the relative susceptibility of C57BL/6 mice to encephalitozoonosis may be due to defective accessory cell function of splenic and peritoneal macrophages, depressed lymphoproliferation against spore fragments (possibly due to prostaglandin-mediated suppression) and a delay in LK production. There was no significant difference between the survival times of BALB/c-nu and C57BL/6-nu mice, suggesting that non-immune mediated resistance did not play a role in determining resistance/susceptibility.