title: Increased severity of Candida vaginitis in BALB/c nu/nu mice versus the parent strain is not abrogated by adoptive transfer of T cell enriched lymphocytes.
abstract: The role of the host immune system in combating candidal infections in the vagina is poorly understood. A murine model of Candida vaginitis was used to elucidate the role of T cells in a candidal infection. Athymic BALB/c nu/nu mice or normal BALB/c mice were induced into estrus and then infected with 1 x 10(6) Candida albicans intravaginally. The infection was monitored over 1 week. Samples from blood, small intestine, tongue, kidney, spleen, liver, uterus and vagina were tested for recoverable C. albicans. Histology of the vagina was assessed for both inflammation and extent of infection. Results indicated that the BALB/c nu/nu mice had similar levels of vaginal yeast load to the normal BALB/c mice. In 25-30% of nude mice Candida was also recovered from extra vaginal sites (kidney, liver, small intestine), however, extra vaginal dissemination was not observed in any normal BALB/c animals. Histologically, both the nu/nu and control BALB/c had similar levels of vaginal inflammation; however, the nu/nu mice had more florid fungal growth in the vaginal epithelium. Adoptive transfer of either immune or non-immune BALB/c T cells into nude mice had no affect on either infection or vaginal inflammation. Immunohistochemical staining of vaginal tissues from normal BALB/c mice or nude mice adoptively transferred with either immune or non-immune T cells with anti-CD3 monoclonal antibody revealed no significant difference between groups in the numbers of CD3+ vaginal T cells. However, in mice receiving either immune or non-immune T cells no yeast was recovered from any tissues except the vagina. These data show that T cells have a limited role in protecting the vagina from C. albicans infection.
authors.affiliation: Department of Obstetrics, Gynaecology and Reproductive Sciences, Magee-Womens Research Institute, Pittsburgh, PA 15213, USA.
authors.forename: C A
authors.initials: CA
authors.lastname: Black
authors.forename: F M
authors.initials: FM
authors.lastname: Eyers
authors.forename: A
authors.initials: A
authors.lastname: Russell
authors.forename: M L
authors.initials: ML
authors.lastname: Dunkley
authors.forename: R L
authors.initials: RL
authors.lastname: Clancy
authors.forename: K W
authors.initials: KW
authors.lastname: Beagley
mesh_terms: D000818:Animals; D002176:Candida albicans / Q000302:isolation & purification; D002181:Candidiasis, Vulvovaginal / Q000209:etiology / Q000276:immunology / Q000382:microbiology / Q000473:pathology / Q000517:prevention & control*; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000276:immunology / Q000382:microbiology; D004958:Estradiol / Q000494:pharmacology; D004971:Estrus; D005260:Female; D016469:Fungemia / Q000209:etiology / Q000276:immunology / Q000628:therapy; D020022:Genetic Predisposition to Disease; D007111:Immunity, Cellular; D007153:Immunologic Deficiency Syndromes / Q000150:complications / Q000628:therapy*; D016219:Immunotherapy, Adoptive; D007377:Interleukin-3 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude / Q000276:immunology*; D012720:Severity of Illness Index; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism / Q000637:transplantation*; D014621:Vagina / Q000276:immunology / Q000382:microbiology / Q000473:pathology
chemical_list: D007377:Interleukin-3; D004958:Estradiol