Inducible immunity to Trichomonas vaginalis in a mouse model of vaginal infection

Abstract

We studied the protective effect of subcutaneous immunization with Trichomonas vaginalis in a mouse model of vaginal infection. BALB/c mice were immunized with various doses of T. vaginalis (4.5 ؋ 10 5 , 9 ؋ 10 6 , and 1 ؋ 10 8 organisms per ml) suspended in Freund's complete adjuvant 56 days prior to vaginal infection and were given booster injections of the same doses of T. vaginalis in Freund's incomplete adjuvant 4 weeks later. Control mice were immunized and given booster injections of phosphate-buffered saline suspended in Freund's complete and incomplete adjuvants. The mice were tail bled and vaginal washes were performed at weekly intervals for 4 weeks to determine the isolation of T. vaginalis and the serum and vaginal antibody reactivity. Mice which had been immunized and given booster immunizations had significantly fewer intravaginal infections and had increased serum and vaginal antibody responses compared with those of control mice (P < 0.01). Mice that were vaginally infected, treated with metronidazole, and then reinfected vaginally did not develop protective immunity. Subcutaneous immunization with whole T. vaginalis organisms appears to confer protection against intravaginal challenge with T. vaginalis, protection which is not achieved as a result of prior vaginal infection.

Immunoglobulin G, Plasma Cells, and Lymphocytes in the Murine Vagina after Vaginal or Parenteral Immunization with Attenuated Herpes Simplex Virus Type 2

“…The available evidence also indicates that IgG antibodies in genital tract secretions are mainly responsible for immune protection against genital tract pathogens. In addition to HSV-2, this has been shown for chlamydiae in guinea pigs (38), C. fetus in cows (8), and trichomonas species in cows (8,9) and mice (1). The evidence of a primary role of secreted IgG antibodies in protection against genital tract infections in females is contrary to the widely accepted paradigm that IgA is the main protective antibody at mucosal surfaces, a discrepancy that has been noted previously by Patton and Rank (36).…”

“…This is evidenced by weak responses to nonreplicating protein antigens (12,26,27,43) and weak responses to natural infections by replicating but noninvasive pathogens that colonize the superficial epithelial cells of the reproductive tract for weeks or months before elimination by an immune response (35). The latter organisms include Campylobacter fetus in cows (10); trichomonas species in cows (8,9), mice (1), and humans (1); Candida albicans in rats and mice (7,13); and papillomaviruses in animals and humans (6,11). Chlamydial infection of the female genital tract in mice and guinea pigs also elicits only a modest convalescent immunity (39), which may be due in part to release of progeny organisms mainly into the genital tract lumen rather than the stroma.…”

Microbiota in vaginal health and pathogenesis of recurrent vulvovaginal infections: a critical review

“…L. acidophilus leads to increase in adherence of T. vaginalis to vaginal epithelial cells, during the early stages of infection [149]. As the number of L. acidophilus increases, the T. vaginalis become incapable of growing, while, vice versa occurs with decrease in number of L. acidophilus at the end of menses and during menopause, consequently leading to increase in TV symptoms [153]. This parasite has also been shown to have damaging effects on L. acidophilus, either by phagocytosis or via proteases [125].…”

The role of immunity in the epidemiology of gonorrhoea, chlamydial infection and trichomoniasis: insights from a mathematical model

“…There is more substantial evidence of immunity in the case of chlamydial infection [17][18][19], although evidence again suggests that immunity is likely to be less significant if treatment is initiated early in infection [20]. In the case of trichomoniasis, there is some evidence suggestive of immunity [21], and it is possible to induce strong immune responses in untreated mice [22].…”