HLA-B27 expression does not modulate intracellular Chlamydia trachomatis infection of cell lines

Chlamydia trachomatis is an obligate intracellular pathogen. Infection of s usceptible individuals with this bacterium can trigger the development of r eactive arthritis, an acute inflammation that is associated with the expres sion of the class I major histo compatibility antigen, HLA-B27. Other facul tative intracellular pathogens, such as Yersinia and Salmonella spp., are a lso known triggers of reactive arthritis. Previous studies report conflicti ng results concerning whether the presence of HLA-B27 modulates the infecti on of cells with these enteric pathogens. In the present study, we have exa mined whether the expression of HLA-B27 can influence the infection of cell lines with C trachomatis and also whether the replication of these bacteri a is altered in HLA-B27-expressing cell lines. To do this, we have used a s ensitive flow cytometric approach. We fixed and permeabilized cells and use d fluorescein isothiocyanate-conjugated monoclonal antibody specific for ch lamydia lipopolysaccharide to detect intracellular bacteria. The staining p attern obtained closely resembled the intracellular life cycle of chlamydia , with the appearance of brightly staining cells correlating to the microsc opic detection of mature inclusion bodies. Moreover, since the percentage o f cells that stained with the antibody was proportional to the infectious i noculum used, we were able to use the technique to quantitate the number of infectious organisms recoverable from infected cell lines. An important co mponent of our study was the use of heparin to prevent reinfection of cells and thus enable the infection to be followed from a discrete time point. O ur results suggest that HLA-B27 influences neither the infection nor replic ation of C. trachomatis serovar L2,within cell lines. Consequently, the rol e of HLA-B27 in the pathogenesis of reactive arthritis may lie downstream o f the invasion and replication stages of the triggering pathogenic infectio n.