Alteration of chlamydia trachomatis biologic behavior in synovial membranes suppression of surface antigen production in reactive arthritis and reiter's syndrome

Abstract

Objective. To investigate the biologic state of Chlamydia and its surface antigen expression in the synovial membranes of patients with Chlamydia‐associated reactive arthritis/Reiter's syndrome (ReA/RS). Methods. Expression of chlamydial lipopoly‐saccharide (LPS), major outer membrane protein (MOMP), and elementary body (EB) antigens was studied by gold labeling immunoelectron microscopy on 6 synovial membrane and 2 synovial fluid (SF) pellet samples from 6 patients with Chlamydia‐associated arthritis. The study findings were compared with 24‐hour cultures of HeLa cells infected with Chlamydia trachomatis EB. Results. Persistent C trachomatis infection was found in all 6 synovial membrane samples from patients who had either early or chronic arthritis. The infection persisted despite antibiotic treatment, including a 1‐month course of doxycycline therapy. Most persistent organisms were atypical reticulate bodies (RBs) found in both fibroblasts and macrophages. Specific, but weak, immunogold staining for all 3 antibodies was found on both intracellular RBs and extracellular EBs. In the SF samples, Chlamydia surface antigens were detected only in phagosomes containing degraded electron‐dense materials. Conclusion. The synovial membrane biopsies conducted in this study of Chlamydia‐associated ReA/RS revealed atypical RBs with diminished MOMP and LPS expression. Such altered organisms may escape immune surveillance and contribute to disease chronicity; moreover, these organisms may be difficult to detect and treat in some ReA/RS patients.

Early cytokine profiles in the joint define pathogen clearance and severity of arthritis in Chlamydia‐induced arthritis in rats

“…Besides the gene sequence for 16S rRNA, Bas et al (26) detected a major outer membrane protein (MOMP) gene sequence and 2 chlamydial plasmid sequences. Several investigators then reported obtaining positive PCR results for 16S rRNA (27,28). Gerard et al (29) took synovial specimens that tested positive for 16S rRNA by PCR and then further identified chlamydial gene products (glyQS, r-protein S5 and L5, and Hsp60) within a majority of these biopsy specimens.…”

Effect of the steroid receptor antagonist RU486 (mifepristone) on an IFNγ-induced persistent Chlamydophila pneumoniae infection model in epithelial HEp-2 cells

“…The presence of C. pneumoniae in persistent infection is characterized by an absence of culturability [7], in addition to altered bacterial RNA and protein levels [8][9][10][11], morphologically altered chlamydial bodies [8] and increased resistance to antimicrobials, such as azithromycin or clarithromycin, frequently used for the treatment of C. pneumoniae infection [12]. The mechanisms leading to persistent C. pneumoniae infection remain unclear; however, infection in reported cases occurred during an uncompleted developmental cycle with a lack of maturation of the EB, and an absence of bacterial metabolic activity caused a decrease in sensitivity to the antibiotics used.…”

Pathogenesis of spondylarthropathies

“…Chlamydia, Yersinia, and Salmonella infect mainly epithelial cells and macrophages, and it is known that they can persist for a long time in macrophages. There is growing evidence that Chlamydia can be detected in synovial fluid and synovial membrane not only in acute, but also in chronic, forms of ReA (42). The detection of chlamydia1 DNA (43) and RNA (42,44) confirms that whole viable organisms are likely to be present.…”

“…There is growing evidence that Chlamydia can be detected in synovial fluid and synovial membrane not only in acute, but also in chronic, forms of ReA (42). The detection of chlamydia1 DNA (43) and RNA (42,44) confirms that whole viable organisms are likely to be present. However, all attempts thus far to find Yersinia DNA in the joint have failed, in spite of the presence of Yersinia antigen detectable by immunologic techniques (45,46).…”