title: Immunization against chlamydial genital infection in guinea pigs with UV-inactivated and viable chlamydiae administered by different routes.
abstract: Female guinea pigs were immunized with viable or UV light-inactivated chlamydiae (agent of guinea pig inclusion conjunctivitis), belonging to the species Chlamydia psittaci, by intravenous, subcutaneous, oral, or ocular routes. All animals were then inoculated vaginally with viable chlamydiae to determine the extent of protection against challenge infection induced by the various regimens. The course of genital infection was significantly reduced in intensity in all groups of animals except the unimmunized controls and those animals immunized orally with inactivated antigen. Guinea pigs immunized with viable antigen were more likely to develop resistance to challenge infection and, in general, had a significantly greater degree of protection than animals immunized with inactivated antigen. No one route seemed superior in producing a protective response. Animals in all groups demonstrating protection developed serum and secretion immunoglobulin G antibody responses to chlamydiae. Lymphocyte proliferative reactions to chlamydial antigen were variable among groups. Immunoblot analysis of serum and secretions indicated a wide range of antibody specificities, but most protected animals produced antibodies to the major outer membrane protein, lipopolysaccharide, and the 61-kilodalton protein. No definitive associations could be made between the increased ability of immunization with viable organisms to produce resistance to challenge infection and a particular immune parameter. These data indicate that viable chlamydiae given by various routes are able to induce a strong immune response which can provide resistance against reinfection in some cases or at least reduce the degree of infection to a greater degree than inactivated antigen. However, complete resistance to genital tract infection may be difficult to obtain and alternate immunizations strategies may have to be developed.
authors.affiliation: Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock 72205.
authors.forename: R G
authors.initials: RG
authors.lastname: Rank
authors.forename: B E
authors.initials: BE
authors.lastname: Batteiger
authors.forename: L S
authors.initials: LS
authors.lastname: Soderberg
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000096:biosynthesis; D000918:Antibody Specificity; D001428:Bacterial Vaccines / Q000008:administration & dosage* / Q000276:immunology; D002690:Chlamydia Infections / Q000276:immunology / Q000517:prevention & control*; D002691:Chlamydophila psittaci / Q000276:immunology* / Q000528:radiation effects; D004195:Disease Models, Animal; D005260:Female; D005831:Genital Diseases, Female / Q000276:immunology / Q000517:prevention & control*; D006168:Guinea Pigs; D007114:Immunization / Q000379:methods; D015151:Immunoblotting; D008213:Lymphocyte Activation / Q000276:immunology; D008214:Lymphocytes / Q000276:immunology; D014613:Vaccines, Attenuated / Q000008:administration & dosage; D015164:Vaccines, Inactivated / Q000008:administration & dosage
chemical_list: D000907:Antibodies, Bacterial; D001428:Bacterial Vaccines; D014613:Vaccines, Attenuated; D015164:Vaccines, Inactivated