Lack of correlation between the detection of Chlamydia trachomatis DNA in synovial fluid from patients with a range of rheumatic diseases and the presence of an antichlamydial immune response.
OBJECTIVE
To resolve how frequently Chlamydia trachomatis and Chlamydia pneumoniae DNA are present in the joints of unselected patients with reactive arthritis (ReA) and undifferentiated oligoarthritis, and to determine if there is an accompanying serologic or cellular antichlamydial immune response.


METHODS
Two polymerase chain reaction (PCR) protocols to detect the plasmid of C. trachomatis and the outer membrane protein 1 gene of C. pneumoniae were developed for specific use with synovial fluid (SF). Subsequently, the assays were used to detect DNA from the 2 organisms in SF from 54 adult patients with rheumatic diseases, including 4 with sexually acquired ReA and 31 with undifferentiated oligoarthritis. The presence of chlamydial antibodies and SF lymphocyte proliferation responses were determined in parallel.


RESULTS
The PCR protocols were species-specific and highly sensitive. SF samples from 15 patients (8 with undifferentiated oligoarthritis, 3 with ReA, 1 with rheumatoid arthritis, and 1 with psoriatic arthritis) were positive for C. trachomatis. There was no significant correlation between the presence of C. trachomatis DNA in the joint and a Chlamydia-specific synovial T cell response or a serologic response. C. pneumoniae was not detected in any of the 54 patients, although it was identified in the SF from a rheumatoid arthritis patient outside this study, demonstrating that the assay was capable of detecting the organism in the joint.


CONCLUSIONS
C. trachomatis DNA was present in ReA patients and in nearly one-third of unselected patients with undifferentiated oligoarthritis, which further supports the hypothesis that it plays an important role in disease pathogenesis. However, its presence did not correlate with evidence of an antichlamydial immune response. Despite previous anecdotal reports, C. pneumoniae does not appear to be a major cause of undifferentiated oligoarthritis or ReA.
Wilkinson
N Z
NZ
University of Southampton, UK.
Kingsley
G H
GH
Sieper
J
J
Braun
J
J
Ward
M E
ME
D000328:Adult; D000907:Antibodies, Bacterial / Q000032:analysis*; D000942:Antigens, Bacterial / Q000276:immunology; D001170:Arthritis, Infectious / Q000276:immunology / Q000382:microbiology*; D002690:Chlamydia Infections / Q000276:immunology / Q000382:microbiology*; D002692:Chlamydia trachomatis / Q000235:genetics* / Q000276:immunology; D016993:Chlamydophila pneumoniae / Q000235:genetics* / Q000276:immunology; D017931:DNA Primers / Q000737:chemistry; D004269:DNA, Bacterial / Q000032:analysis*; D005260:Female; D006801:Humans; D008213:Lymphocyte Activation; D008297:Male; D016133:Polymerase Chain Reaction; D000091402:Prohibitins; D013582:Synovial Fluid / Q000276:immunology / Q000382:microbiology*; D013601:T-Lymphocytes / Q000276:immunology
D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D017931:DNA Primers; D004269:DNA, Bacterial; C000717331:PHB2 protein, human; D000091402:Prohibitins