Role of endogenous gamma interferon in host defense against Chlamydia trachomatis infections

Abstract

BALB/c mice (6 to 8 weeks old) infected with Chlamydia trachomatis serovar L1 were sacrificed, and the yield of Chlamydia inclusion-forming units from the liver and lungs was measured in HeLa 229 cells. The yield of inclusion-forming units reached a peak at 3 days postinfection and then progressively declined. The mice infected with C. trachomatis had no detectable levels of gamma interferon (IFN-gamma) in their sera. However, stimulation of their spleen cells with either concanavalin A or heat-killed C. trachomatis resulted in the release of high levels of IFN-gamma (600 to 900 IU/ml) at 5 to 8 days postinfection. The increased release of IFN-gamma from the spleen cells paralleled the clearance of chlamydia from the liver and lungs. Sera and spleen cells from animals immunized with live C. trachomatis were transferred to recipient mice that were subsequently challenged with C. trachomatis. Transfer of spleen cells resulted in a reduction of the infection in the recipient animal as measured by the yield of chlamydia from the spleen, but transfer of the sera did not confer protective immunity. In addition, mice infected with C. trachomatis serovar L1 were treated with a hamster neutralizing monoclonal antibody to recombinant murine IFN-gamma (MAb-MuIFN-gamma). In the animals receiving the MAb-MuIFN-gamma, the yield of chlamydia from the lungs, spleen, and liver was significantly higher than from the control groups of mice. Histopathological analysis of tissues from the chlamydia-infected mice showed that the animals treated with the MAb-MuIFN-gamma had a significantly more extensive inflammatory reaction in their lungs, liver, and spleen.