Susceptibility of IFN-γ or IL-12 knock-out and SCID mice to infection with two microsporidian species, Encephalitozoon cuniculi and E. intestinalis

Abstract

Susceptibility of three strains of immunodeficient mice to two related microsporidian species Encephalitozoon cuniculi Levaditi, Nicolau et Schoen, 1923 and Encephalitozoon intestinalis (Cali, Kotler et Orenstein, 1993) was compared. While both, severe combined immunodeficient (SCID) and interferon-gamma knock-out (IFN-gamma KO) mice, succumbed to either intraperitoneal (i.p.) or peroral (p.o.) (natural) infection with both parasites, only i.p. infection with E. cuniculi killed interleukin-12 knock-out (IL-12 KO) mice. IFN-gamma KO mice died earlier than SCID mice. Adoptive transfer of naive splenocytes from IFN-gamma KO mice did not protect the SCID mice from a lethal infection with either of the Encephalitozoon species. However, reconstituted mice survived significantly longer (P<0.05), thus indicating the role of IFN-gamma produced by host NK cells in the development of mechanisms of anti-microsporidial protective immunity. Non-lethal outcome of the infection always correlated with the increase in CD8+ T lymphocyte subpopulation. Both E. intestinalis-infected IFN-gamma KO and IL-12 KO mice produced comparable levels of specific antibodies, suggesting that antibodies did not protect IFN-gamma KO mice from lethal infection.