Prior genital tract infection with a murine or human biovar of Chlamydia trachomatis protects mice against heterotypic challenge infection

We sought to assess the degree of cross-protective immunity in a mouse mode l of chlamydial genital tract infection. Following resolution of genital in fection with the mouse pneumonitis (MoPn) biovar of Chlamydia trachomatis, mice were challenged intravaginally with either MoPn or human serovar E or L2. The majority of animals previously infected with MoPn were solidly immu ne to challenge with either of the two human biovars. Surprisingly, approxi mately 50% of animals became reinfected when homologously challenged with M oPn, although the secondary infection yielded significantly lower numbers o f the organism isolated over a shorter duration than in the primary infecti on. Primary infection with serovar E also protected against challenge with MoPn or serovar L2, although the degree of immune protection was lower than that resulting from primary infection with MoPn. Blast transformation and assessment of delayed-type hypersensitivity indicated that mice previously infected with either human or murine biovars produced broadly cross-reactiv e T cells that recognized epitopes of either murine or human biovars of C. trachomatis. Immunoblotting demonstrated that primary MoPn infection produc ed immunoglobulin G (IgG) antibody to antigens of MoPn as well as at least three distinct antigenic components of human serovar E, one of which was id entical in molecular weight to the major outer membrane protein (MOMP). Pri mary infection with serovar E produced IgG antibody reactive against serova r E but not MoPn MOMP and against at least one ca. 60-kDa protein of both c hlamydial strains. Our results indicate that primary genital infection of m ice with murine C. trachomatis induces immunity against challenge with eith er of two human biovars.