title: Role of cell-mediated immunity in the resolution of secondary chlamydial genital infection in guinea pigs infected with the agent of guinea pig inclusion conjunctivitis.
abstract: Guinea pigs which have recovered from a genital infection with the agent of guinea pig inclusion conjunctivitis demonstrate strong immunity to reinfection for a short period of time but then become susceptible to reinfection. The secondary infection is markedly shortened in duration and decreased in intensity. Previous studies have indicated an important role for humoral immunity in resistance to and in recovery from reinfection. However, the contribution of cell-mediated immunity to immunity toward or recovery from a secondary infection is not clear. Guinea pigs were infected in the genital tract with guinea pig inclusion conjunctivitis and were challenged at either 30 or 75 days after the primary infection. Prior to challenge, one group of animals were injected with rabbit anti-guinea pig thymocyte serum (ATS) while control groups received either normal rabbit serum or no treatment. Treatment was continued daily for the course of the experiment. On day 30, ATS-treated guinea pigs had a slightly higher rate of reinfection, and generally the infection persisted longer than in controls. On day 75, all animals became reinfected upon challenge, but control animals resolved their infections in 3 to 9 days. In contrast, most ATS-treated animals remained infected throughout the course of the experiment. Although the animals became reinfected, the levels of chlamydiae were much lower than those observed during the primary infection. ATS treatment abrogated T-cell responses, but serum and secretory antibody responses remained normal. Histopathological examination revealed some decrease in mononuclear infiltration of endocervical and uterine tissues in ATS-treated animals. These data indicate that previously infected guinea pigs require both cell-mediated immunity and humoral immunity for resolution of a challenge infection.
authors.affiliation: Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock 72205-7199.
authors.forename: R G
authors.initials: RG
authors.lastname: Rank
authors.forename: L S
authors.initials: LS
authors.lastname: Soderberg
authors.forename: M M
authors.initials: MM
authors.lastname: Sanders
authors.forename: B E
authors.initials: BE
authors.lastname: Batteiger
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000096:biosynthesis; D000961:Antilymphocyte Serum / Q000627:therapeutic use; D002584:Cervix Uteri / Q000276:immunology / Q000473:pathology; D002690:Chlamydia Infections / Q000276:immunology* / Q000628:therapy; D002692:Chlamydia trachomatis / Q000276:immunology*; D005260:Female; D006168:Guinea Pigs; D007111:Immunity, Cellular; D007071:Immunoglobulin A, Secretory / Q000276:immunology; D007156:Immunologic Memory; D007167:Immunotherapy; D013997:Time Factors; D014621:Vagina / Q000276:immunology / Q000473:pathology
chemical_list: D000907:Antibodies, Bacterial; D000961:Antilymphocyte Serum; D007071:Immunoglobulin A, Secretory