Anti-C. trachomatis MOMP Monoclonal antibody, Clone 23-777.44.4

Male chlamydial infections are becoming more recognised as an aetiological agent in infertility. An IFN-gamma response is required for protection against Chlamydia in females, but may have the potential to induce pathology in the immune-privileged male reproductive tract. We examined the induction of immunity following intranasal immunisation with major outer membrane protein (MOMP) of Chlamydia muridarum in male BALB/c mice, and the role of MOMP-specific CD4(+) T cells in clearance of an intrapenile infection. Here we report that adoptive transfer of MOMP-specific CD4(+) T cells into naive mice confers partial protective immunity, which significantly reduces the tissue burden of Chlamydia. (C) 2010 Elsevier Ltd. All rights reserved.

Microbial interactions represent an understudied facet of human health and disease. In this study, the interactions that occur between Chlamydia trachomatis and the opportunistic fungal pathogen, Candida albicans were investigated. Candida albicans is a common component of the oral and vaginal microbiota responsible for thrush and vaginal yeast infections. Normally, Candida exist in the body as yeast. However, disruptions to the microbiota create conditions that allow expanded growth of Candida, conversion to the hyphal form, and tissue invasion. Previous studies have shown that a myriad of outcomes can occur when Candida albicans interacts with pathogenic bacteria. To determine if C. trachomatis physically interacts with C. albicans, we incubated chlamydial elementary bodies (EB) in medium alone or with C. albicans yeast or hyphal forms for 1 h. Following incubation, the samples were formaldehydefixed and processed for immunofluorescence assays using anti-chlamydial MOMP or anti-chlamydial LPS antibodies. Replicate samples were replenished with culture medium and incubated at 35 degrees C for 0-120 h prior to fixation for immunofluorescence analysis or collection for EB infectivity assays. Data from this study indicates that both C. trachomatis serovar E and C. muridarum EB bind to C. albicans yeast and hyphal forms. This interaction was not blocked by pre-incubation of EB with the Candida cell wall components, mannan or beta-glucans, suggesting that EB interact with a Candida cell wall protein or other structure. Bound EB remained attached to C. albicans for a minimum of 5 days (120 h). Infectivity assays demonstrated that EB bound to C. albicans are infectious immediately following binding (0h). However, once bound to C. albicans, EB infectivity decreased at a faster rate than EB in medium alone. At 6h post binding, 40% of EB incubated in medium alone remained infectious compared to only 16% of EB bound to C. albicans. Likewise, pre-incubation of EB with laminarin, a soluble preparation of beta-glucan, alone or in combination with other fungal cell wall components significantly decreases chlamydial infectivity in HeLa cells. These data indicate that interactions between EB and C. albicans inhibit chlamydial infectivity, possibly by physically blocking EB interactions with host cell receptors.