Heterotypic protection of mice against chlamydial salpingitis and colonization of the lower genital tract with a human serovar F isolate of Chlamydia trachomatis by prior immunization with recombinant serovar L1 major outer-membrane protein.

Intrauterine infection of mice with a human genital tract isolate of Chlamydia trachomatis (serovar F) resulted in salpingitis. In some cases, oviduct damage was sufficient to cause infertility due to lumenal blockage. Parenteral immunization with a purified, heterologous, recombinant major outer-membrane (rMOMP) preparation reduced the proportion of animals developing severe salpingitis by 77% compared with mock-immunized controls, but failed to reduce chlamydial colonization of the lower genital tract. In contrast, mice immunized with rMOMP directly into the Peyer's patches to stimulate mucosal immunity shed fewer chlamydiae from the vagina than controls, but showed little reduction in oviduct damage. No consistent correlation was observed between antibody levels to rMOMP in immunized mice and reduced lower genital tract colonization. Immunization with rMOMP via the presacral space, a route previously shown to stimulate mucosal immunity in the genital tract, produced high levels of circulating anti-rMOMP IgG but only traces of anti-rMOMP IgA in vaginal secretions. There was no difference in the severity of salpingitis in these animals compared with mock-immunized controls. Immunization with rMOMP conferred no protection against infertility resulting from direct inoculation of chlamydiae into the oviducts.