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Infect Immun. 1990 November; 58(11): 3553-3557

Reduced lymphocyte responses to mitogens in natural and experimental trichomoniasis.

Department of Medical Microbiology, University of Zimbabwe Medical School, Harare.

ABSTRACT

Proliferative responses to mitogens were determined by using peripheral blood mononuclear cells from women with active trichomoniasis, with serological evidence of past infection with Trichomonas vaginalis, and with no evidence of current or past infection. Even after the human immunodeficiency virus antibody status of the patients was taken into account, cells from women with active trichomoniasis showed reduced responses to phytohemagglutinin, concanavalin A, pokeweed mitogen, and bacterial lipopolysaccharide. Similar findings were obtained by using spleen cells from mice inoculated subcutaneously with live trichomonads. Reduction in proliferative responses by these cells could be detected 3 days after inoculation. There was some evidence to suggest that more-pathogenic strains of the parasite induced a greater degree of immunosuppression. The responses of spleen cells from mice inoculated with trichomonad-free culture supernatants were within normal limits, indicating that live trichomonads were needed to induce suppression. Support for this was gained from studies with cells from women who were treated successfully. Cells from these women rapidly regained normal lymphoproliferative function. Interleukin-2 (IL-2) production by spleen cells from infected mice was determined from measurements of mitochondrial activity in an IL-2-dependent T-cell line following incubation with stimulated spleen cell culture supernatants. These tests demonstrated lower IL-2 activity in supernatants from cell cultures from infected mice than in those from uninfected mice. The reduction in IL-2 activity did not, however, appear to correlate with the degree of reduction of mitogen-induced lymphoproliferation. Suppression of T-cell-mediated immunity may be one of the mechanisms by which T. vaginalis is able to evade host responses to infection.