Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antibodies to Salmonellae, Yersiniae, Campylobacter jejuni, Borrelia burgdorferi, Klebsiella pneumoniae, Escherichia coli, Proteus mirabilis and Chlamydia trachomatis were measured by ELISA in the sera of 99 patients with ankylosing spondylitis. Increased prevalence of IgA and IgG class antibodies against K. pneumoniae and of IgA class against E. coli was observed in ankylosing spondylitis. No clear correlation between the disease activity and occurrence of antibodies was revealed. The results are in line with the previously published findings suggesting that K. pneumoniae may have a role in the aetiopathogenesis of ankylosing spondylitis.
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PMID:Bacterial antibodies in ankylosing spondylitis. 204 28

Pathogenesis of seronegative spondyloarthropathies such as ankylosing spondylitis and reactive arthritis is not known. Growing evidence indicates that microbial structures such as Chlamydia antigen and Yersinia antigen are present in the inflamed joints of patients with reactive arthritis. Microbial antigens can activate the host's inflammatory mechanisms. After the activation, the course of inflammation can be postulated to be affected by the host factors responsible for amplification of the inflammatory reaction and elimination of the foreign structures. Thus, the amplification, whether strong, moderate, or weak, may contribute to the degree of inflammatory tissue injury in patients with seronegative spondyloarthropathies. This review will discuss the role of increased inflammatory reactivity in the pathogenesis of HLA-B27 associated spondyloarthropathies, with special reference to reactive arthritis triggered by yersinia enteritis.
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PMID:Enhanced inflammatory reactivity in the pathogenesis of spondyloarthropathies. 210 68

Antibodies to Chlamydia trachomatis were found in 60% of patients with reactive arthritis (ReA) and 33% of patients with ankylosing spondylitis (AS), compared with 19% of healthy blood donors. The IgG, IgA and IgM immune responses in patients with ReA and AS were further analysed by immunoblotting. Most patients had IgG antibodies to a large number of C. trachomatis antigens. IgA (and especially IgM) antibodies were less prevalent. Differences in the antibody response to individual antigens were seen between the two groups of patients, with respect to both IgG and IgA. Especially evident was the high prevalence of IgA antibodies to a 60 kD antigen among patients with ReA (67%) compared with patients with AS (20%).
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PMID:Immunoblot analysis of antibody response to Chlamydia trachomatis in patients with reactive arthritis and ankylosing spondylitis. 261 27

A cohort analytic study was performed to investigate serum IgA-class antibodies against Chlamydia in 24 patients with chlamydial-induced arthritis (CIA). IgA-class antibodies against chlamydial antigens were positive (titre greater than or equal to 1:16) in 23 of the 24 IgG-positive CIA-patients (96%) in contrast to 16 of 40 patients (40%) with other rheumatic diseases (ankylosing spondylitis n = 6; undifferentiated arthritis n = 11; rheumatoid arthritis n = 12; degenerative joint disease n = 11), also positive for IgG-class chlamydial antibodies. Both the presence of specific IgA-antibodies and their geometric mean titre (1:28 vs. 1:4) differed significantly (p less than 0.001) between the two groups.
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PMID:Specific serum IgA-antibodies in chlamydial-induced arthritis. 273 57

Demonstration of chlamydial antibodies in patients with ankylosing spondylitis (AS) could show an etiological role of Chlamydia trachomatis in this condition. We studied serum specimens from 50 HLA-B27 positive patients with AS (Group I), 34 HLA-B27 positive patients with other rheumatic diseases (Group II), 67 HLA-B27 positive healthy blood donors (Group III) and 37 healthy untyped blood donors. (Group IV). Measured by an immunoperoxidase assay (IPA) chlamydial IgA (titre greater than or equal to 1:20) was more prevalent in the HLA-B27 positive persons than in the healthy controls not selected for HLA-group (Groups I + II + III vs IV : p less than 0.02). Chlamydia trachomatis IgA-IPA containing sera also had specific IgG-IPA antibodies (greater than or equal to 1:80) in 29 (96%) out of 30 sera from HLA-B27 positive individuals and controls. Conversely, 45% of specific IgG-positive (greater than or equal to 1:80) AS sera, 27.7% sera in Group II, 39.4% Group III sera vs. 11.1% of sera in Group IV had concomitant chlamydial IgA (greater than or equal to 1:20). The differences in the prevalence of specific IgA were statistically significant: Group I vs. IV : p less than 0.01; Group III vs. IV :p less than 0.05 and Gr. I + II + III vs. IV: p less than 0.05. Our data suggest an enhanced antibody production against Chlamydia trachomatis among the HLA-B27 positive individuals whether they have AS or are healthy.
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PMID:Chlamydia trachomatis serology in ankylosing spondylitis. 332 42

We have previously reported the association of Chlamydia trachomatis with HLA B27+ related diseases. To investigate the possibility that chlamydial antibodies serve to localize the immune response in such diseases, we examined the crossreactivity of chlamydial antibodies (rabbit anti-D and anti-L2 serotypes) with peripheral blood mononuclear cells of patients with ankylosing spondylitis (AS) and anterior uveitis (AU) and with human and bovine ocular tissue and cells in culture. Our results indicate a significantly increased percentage binding of chlamydial antibody (D serotype) to the mononuclear cells of HLA B27+ patients with AS when compared with HLA B27- patients with AS (12.9% +/- 2.2 versus 5.4% +/- 2.2), B27+ controls (5.5% +/- 1.5) and B27- controls (6.1% +/- 1.0). There was no significant difference between controls and HLA B27+ patients with AU (6.6% +/- 1.9) and B27- patients with AU (8.7% +/- 1.1). This crossreactivity could not be blocked by monoclonal HLA B27 antibody. Chlamydial antibodies (D and L2) crossreact with human and bovine conjunctiva but not uvea, tissue culture derived iris fibroblasts or smooth muscle cells. Our results provide additional support for the concept of crossreactivity between antibodies to microbial agents and peripheral blood mononuclear cells of patients with HLA B27+ AS.
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PMID:Chlamydial antibody crossreactivity with peripheral blood mononuclear cells of patients with ankylosing spondylitis: the role of HLA B27. 348 86

The pathogenic links between HLA antigens, certain bacterial infections and arthritis have not yet been characterized. The hypothesis of cross-reactivity between HLA B27, the marker of disease susceptibility for these disorders, and the provocative microorganism has been suggested by studies of Klebsiella and ankylosing spondylitis. The present study examines the possibility of molecular mimicry between HLA B27 and two organisms implicated more directly in reactive arthritis, Yersinia enterocolitica and Chlamydia trachomatis. Antibodies against these organisms were obtained both from patients and from antisera raised in rabbits. Neither source of antibacterial antibody was specifically cytotoxic for HLA B27-positive lymphocytes, even when the target cells were derived from patients with recent infections due to these organisms. In addition, monoclonal antibodies against HLA B27 (M1 and M2) showed no reactivity with antigens from these organisms in an ELISA system. These data do not support the notion of molecular mimicry as being the basis of immunogenetic susceptibility to reactive arthritis and Reiter's syndrome following infections with Y. enterocolitica and C. trachomatis.
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PMID:Molecular mimicry in Reiter's syndrome: cytotoxicity and ELISA studies of HLA-microbial relationships. 348 63

146 men with rheumatoid factor-negative (sero-negative) arthritis, i.e., 97 patients with ankylosing spondylitis, 36 patients with Reiter's syndrome, and 13 patients with reactive arthritis, were examined for infections of the urogenital tract by following recently established criteria. 74 patients (50.7%) had infections of the male adnexes: 3 patients suffered from balanitis, 14 patients from urethritis, 49 patients from prostatitis, 1 patient from epididymitis, and 7 patients from urinary tract infection. Balanitis and urethritis were almost exclusively associated with Reiter's syndrome. In 37 of 97 patients with ankylosing spondylitis, a urogenital tract infection, mainly a prostatitis (31 patients), was detected. The microorganisms isolated most frequently from patients suffering from urethritis and prostatitis, were Chlamydia trachomatis and Ureaplasma urealyticum.
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PMID:Rheumatoid factor-negative arthritis, especially ankylosing spondylitis, and infections of the male urogenital tract. 665 36

Thirty male patients with sexually acquired reactive arthritis (SARA) have been studied at the time of their initial presentation and thereafter. Chlamydia trachomatis was isolated from the urethral exudate of 9 (36.0%) of the 25 patients from whom urethral specimens were taken, and elevated titres of IgM antibody of C. trachomatis were detected in 11 (36.6%) of the 30 initial sera. Thirteen (43.3%) of the patients has a positive urethral culture and/or elevated titre of IgM antibody, and it is therefore suggested that 43.3% of these patients suffered an acute chlamydial infection at or near the time of the onset of their joint disease. The demonstration of 4-fold or greater rises and/or falls in IgM antibody titre (8 patients) and IgG antibody titre (6 patients) in a group of 15 men studied throughout the course of their disease strongly supports this conclusion. A positive urethral culture and/or raised titre of IgM serum antibody was also detected in 25 (50%) of 50 men with uncomplicated nongonococcal urethritis (NGU), suggesting that the prevalence of chlamydial infections in the 2 conditions is similar. Titres of IgG serum antibody to C. trachomatis were, however, significantly higher in patients with SARA than in those with NGU or other rheumatic diseases, and in healthy controls. The geometric mean titres (GMT) of IgG serum antibody in patients with SARA, NGU, rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus, and in healthy controls were 1:47.5, 1:8.6, 1:2.2, 1;2.2, 1:3.5, and 1:1.4, respectively. These findings suggest that an exaggerated antibody response to acute infection by C. trachomatis may be an important factor in the development of SARA in some but not all patients.
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PMID:Evidence of Chlamydia trachomatis infection in sexually acquired reactive arthritis. 689 52

In the pathogenesis of reactive arthritis, infection through the mucosal route and genetic susceptibility (HLA-B27) are the most important contributing factors. With regard to non-specific urethritis, most probably caused by Chlamydia trachomatis infection, the use of early antimicrobial therapy has been shown to be effective in preventing arthritic recurrences. When the arthritis has been initiated, short-term conventional antimicrobial therapy seems unable to modify the course of the ongoing disease. In patients with acute reactive arthritis, a prolonged (3-month) treatment with tetracycline shortens the duration of arthritis when triggered by Chlamydia trachomatis, while such treatment has not proved effective in enteroarthritis. In patients with chronic reactive enteroarthritis, a prolonged course of quinolones, such as ciprofloxacin, might be of benefit. Sulfasalazine, which has an effect in the acute exacerbations of ankylosing spondylitis, is probably also effective in chronic reactive arthritis. An antimicrobial effect can be one of the mechanisms by which sulfasalazine exerts its therapeutic effect. Follow-up studies are necessary to assess the influence of antibiotic therapy on the late prognosis of patients with reactive arthritis.
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PMID:Are antibiotics of any use in reactive arthritis? 810 15


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