Anti-C. trachomatis MOMP Polyclonal antibody[Biotin]

Antibodies that neutralize infectivity are directed at the antigenically variant major outer membrane protein (MOMP) of Chlamydia trachomatis. A vaccine for chlamydia will need to include T cell determinants that elicit T helper (Th) cells which provide help to MOMP-specific B cells. A limited number of determinants on MOMP are able to elicit Th cells and sequence diversity in the MOMP molecule may alter T cell recognition of these determinants. We investigated whether two sequence invariant proteins of C trachomatis that are both abundant and immunogenic could elicit T cell help for the production of antibody to MOMP We found that outer membrane protein 2 (OMP2) but not outer membrane protein 3 (OMP3) was able to prime BALB/c mice for an anamnestic anti-MOMP response following boost with the intact organism. This demonstration of an intermolecular mechanism of T cell help in a bacterial system has important implications for the development of a chlamydial vaccine as well as the design of vaccines for other antigenically variant non-viral pathogens.

We sought to assess the degree of cross-protective immunity in a mouse model of chlamydial genital tract infection. Following resolution of genital infection 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 immune to challenge with either of the two human biovars. Surprisingly, approximately 50% of animals became reinfected when homologously challenged with MoPn, although the secondary infection yielded significantly lower numbers of the organism isolated over a shorter duration than in the primary infection. 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-reactive T cells that recognized epitopes of either murine or human biovars of C. trachomatis. Immunoblotting demonstrated that primary MoPn infection produced 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 identical in molecular weight to the major outer membrane protein (MOMP). Primary infection with serovar E produced IgG antibody reactive against serovar E but not MoPn MOMP and against at least one ca. 60-kDa protein of both chlamydial strains. Our results indicate that primary genital infection of mice with murine C. trachomatis induces immunity against challenge with either of two human biovars.