Genital and Systemic Immune Responses in a Murine Model of Tritrichomonas foetus Infection

Abstract

A reliable laboratory animal model would be useful for the study of immune responses to trichomoniasis, a sexually transmitted disease of human beings and cattle. Murine models are available, but pretreatment with estrogen is used, which may influence immune responses. To evaluate whether vaginal trichomoniasis could be established in nonestrogenized mice and to define the immune responses associated with the infection, CD1 and BALB/c mice were studied with or without estrogen treatment prior to inoculation with Tritrichomonas foetus. Tritrichomonas Foetus was cultured from the vagina and uterus of both estrogen-treated and untreated control mice for up to 26 wk. The infection was sustained better in BALB/c than in CD1 mice, suggesting that the former strain was most susceptible. In CD1 mice, infection was sustained less well in estrogen-treated than in untreated control mice, but there was no difference between treatment groups of BALB/c mice. IgA and IgG antibodies in vaginal secretions, uterine secretions, and serum specific for a surface antigen of T. foetus (TF1.17) were measured by enzyme-linked immunosorbent assay. In infected CD1 mice, vaginal IgA and IgG antibodies were detected by 8 wk postinoculation (PI). In infected BALB/c mice, vaginal IgA and IgG antibodies were detected by 12 wk PI. Uterine IgG responses predominated over IgA in estrogen-treated and untreated CD1 and BALB/c mice. There were high levels of IgG, but relatively no IgA in the sera of CD1 and BALB/c mice. Overall, the highest IgA response was in the vaginal secretions of infected CD1 mice, and some animals of this strain cleared the infection. These results show that a chronic trichomonad infection was established in mice without prior treatment with estrogen. The infection was associated with antibody responses in reproductive secretions and serum. This animal model will be useful in studying immunization to protect against trichomoniasis in mice not immunocompromised by estrogen.