Resistance to Encephalitozoon intestinalis is associated with interferon-gamma and interleukin-2 cytokines in infected mice

The understanding of the immunopathology of infections caused by microspori dia has pinpointed the importance of T cell-mediated immunity The immunopat hology caused by the interesting protozoan parasite Encephalitozoon intesti nalis, a microsporidium pathogenic in man, is not clearly understood. In th is study, we demonstrate that a specific cellular immune response is implic ated in the control of microsporidiosis infection in mice. Interferon (IFN) -gamma receptor knockout mice (IFN-gamma R-o/o) developed a chronic infecti on with E. intestinalis, whereas a transient infection developed in wild-ty pe mice. Encephalitozoon intestinalis proteins induced proliferation of mur ine spleen and mesenteric lymph node cells collected from infected mice. Th e host response to microsporidia infection was regulated by a specific patt ern of cytokine protection. Spleen cells derived from resistant 129 Sv/Ev m ice inoculated with E. intestinalis secreted significant levels of gamma -i nterferon and interleukin-2 bur cells from highly susceptible IFN-gamma R k nockout mice secreted high levels of interleukin-4 (mostly between 2 and 4 weeks post infection). This is the first report in which a specific cellula r immune response against E. intestinalis infection is presented.