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 proteus species were measured in patients with rheumatoid arthritis (RA) and ankylosing spondylitis (AS) and in healthy controls by a Coombs agglutination method. The titres to Proteus mirabilis were higher in 30 RA patients being treated with gold than in 24 patients with active AS (p less than 0.001), 28 patients with inactive AS (p less than 0.001), and 41 healthy control subjects (p less than 0.001). Control studies with Klebsiella pneumoniae var oxytoca showed high antibody titres only in active AS patients.
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PMID:Antibodies to proteus in rheumatoid arthritis. 286 70

Antibodies to Klebsiella, but not to other bacteria, have been shown to be present in patients with active ankylosing spondylitis (AS) by seven different techniques. Antibodies to Proteus, but not to E. coli or Klebsiella, have been shown to be present in patients with active rheumatoid arthritis (RA) by three different techniques. It is suggested AS and RA are forms of reactive arthritis, to Klebsiella and Proteus respectively, probably mediated by cross-reactivity to HLA antigens.
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PMID:Klebsiella antibodies in ankylosing spondylitis and Proteus antibodies in rheumatoid arthritis. 304 77

Antibodies to Klebsiella oxytoca and Proteus mirabilis in 21 active ankylosing spondylitis (AS), 13 active rheumatoid arthritis (RA), 19 inactive RA patients and 18 healthy controls were measured using enzyme-linked immunosorbent assay (ELISA). Elevated anti-Klebsiella antibodies were demonstrated in active AS patients compared to active RA (p less than 0.01), inactive RA patients (p less than 0.001) and controls (p less than 0.005). When measuring antibodies to Proteus, active RA patients showed higher levels of antibodies compared to active AS patients (p less than 0.005) and healthy controls (p less than 0.05). Further investigations are required to assess the role of Klebsiella and Proteus microorganisms in AS and RA respectively.
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PMID:Antibodies to Klebsiella and Proteus microorganisms in ankylosing spondylitis and rheumatoid arthritis patients measured by ELISA. 304 78

Serological studies on ankylosing spondylitis (AS; N = 82) show that although statistically more AS patients than controls (N = 24) may possess elevated serum titres to enterobacteria such as Salmonella, Shigella and Yersinia, this does not necessarily imply enterobacterial involvement in AS, as other groups without enteritis or arthropathies that frequent health care facilities (N = 72) may also display this phenomenon, presumably due to increased exposure. Moreover, an inventory of all detectable antibody reactivities to the separated cell envelope antigens of five enterobacterial species suspected of involvement in AS (notably Enterobacter, Klebsiella, Salmonella, Shigella and Yersinia) failed to reveal statistical associations with AS. This might be explained, assuming that the aetiology of AS entails a set of enterobacteria rather than a few individual species. It is proposed that serological studies on AS should be supported by additional information, e.g. that of the faecal carriage, and that these combined studies encompassing other enterobacteria, in addition to Klebsiella, might be fruitful.
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PMID:Antibodies to Enterobacteriaceae in ankylosing spondylitis. 309 49

The lymphocyte response of mononuclear cells (MNC) to Klebsiella (Klebs) was studied in ankylosing spondylitis (ASP) and, for comparison, in patients convalescing from Klebs infection and in HLA-B27+ and B27- healthy blood donors. When large doses of various Klebs cell envelope structures were used, MNC from all healthy blood donors were stimulated to produce LIF but not to synthesize significant amounts of DNA. In contrast, MNC from convalescent patients showed LIF synthesis (but no significant proliferation) even when small doses of the Klebs biostructures were used. This heightened LIF response to Klebs was long-standing and could be demonstrated even after serum antibodies had vanished. Very similarly, MNC from ASP patients did not proliferate significantly, but could be activated to produce LIF even with small doses of Klebs. The heightened LIF response to Klebs in ASP appeared to be correlated with the clinical activity and/or duration of the disease. In contrast, there was no correlation between the presence of HLA-B27 in ASP patients or healthy controls and the LIF or proliferative response to Klebs.
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PMID:Lymphocyte response to Klebsiella in ankylosing spondylitis. 310 Feb 99

Twenty three anti-Klebsiella antisera were tested for their cytotoxic activity and four for their binding capacity for peripheral blood lymphocytes (PBL) from patients with HLA-B27 positive ankylosing spondylitis (AS+B27+) and from B27 positive (AS-B27+) and B27 negative (AS-B27-) healthy individuals. None of the antisera showed specific activity against PBL from any particular group. The antisera tested included two anti-Klebsiella K43 sera provided by an Australian group, who have reported them to be specifically cytotoxic for AS+B27+ PBL, four antisera raised against a Klebsiella K43 strain provided by this group, and an antiserum from another group, who have reported it as having increased binding capacity for AS+B27+ and AS-B27+ PBL compared with AS-B27- PBL. The results of other workers who have attempted to reproduce the results of either group are reviewed and the possible reasons for the repeated failure to confirm the reported findings are discussed.
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PMID:Ankylosing spondylitis, HLA-B27, and Klebsiella: a study of lymphocyte reactivity of anti-Klebsiella sera. 348 8

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

Recent studies have indicated that both ankylosing spondylitis and the anti-DNA antibodies found in systemic lupus erythematosus may be related to Klebsiella surface antigens. In order to explore these possible relationships further, the sera of 24 patients with ankylosing spondylitis (AS), and 20 controls, have been examined for binding to a wide range of antipolynucleotide antibodies, antibodies binding to the Klebsiella pneumoniae polysaccharide K30 and two DNA antibody idiotypes designated 16/6 and 134. We report that although 21% of the AS patients had IgG ssDNA antibodies it is evident that the aetiopathogenesis of this disease is not through the mechanism of autoantibodies or the common DNA antibody idiotypes tested.
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PMID:A study of antipolynucleotide antibodies, anti-Klebsiella (K30) antibodies and anti-DNA antibody idiotypes in ankylosing spondylitis. 349 12

Enteric infections with Gram-negative bacteria are thought to play an important part in HLA-B27-associated disease such as Reiter's syndrome and reactive arthritis. But the role of bacterial infections in HLA-B27-positive ankylosing spondylitis (AS) and acute anterior uveitis (AU) is still controversial. A special interest has recently been devoted to the role of klebsiella infection in HLA-B27-associated disease. We studied the humoral immune response against a 'cross-reactive' strain of Klebsiella pneumoniae in 62 patients with anterior uveitis and 33 healthy controls. The anterior uveitis patients were subdivided into 25 HLA-B27-negative patients without AS (B27- AU+ AS-), 17 HLA-B27-positive patients without ankylosing spondylitis (B27+ AU+ AS-), and 19 HLA-B27-positive patients with ankylosing spondylitis (B27+ AU+ AS+). Total serum IgA was higher in patients than in controls in both the B27+ AU+ AS+ and B27+ AU+ AS- patients but not in the B27- AU+ AS- group. No abnormalities were observed in the total serum IgG levels. The level of both the IgG and IgA klebsiella antibodies did not differ in the various patient groups tested as compared with the controls. Comparisons between the patient groups showed that the IgG anti-klebsiella response was higher in B27-positive patients patients without AS than in those with AS. These results suggest that stimulation of mucosal surfaces may play a role in HLA-B27-associated anterior uveitis. Whether klebsiella organisms are involved in this stimulation remains unclear.
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PMID:IgG and IgA immune response against klebsiella in HLA-B27-associated anterior uveitis. 351 61

A component of the cell walls of certain enteric bacteria has been identified that cross-reacts with an HLA-B27-associated cell-surface structure on lymphocytes and other cell types from patients with ankylosing spondylitis. This component, or "modifying factor," from one particular organism, Klebsiella K43-BTS1, has been studied in detail. A purification scheme has been developed using preparative electrofocusing and gel-permeation high performance liquid chromatography techniques and the purified material used in various characterization studies. A previous study demonstrated that the modifying factor has an approximate molecular weight of 30,000 and an isoelectric point of 5.4-5.5. In this study two-dimensional gel electrophoresis experiments demonstrated that the modifying factor is associated with a single protein component of the cell wall of this organism. Pronase and papain destroyed the modifying factor activity whereas trypsin and alpha-chymotrypsin degraded the factor into smaller fragments without destroying its ability to modify B27+ AS- lymphocytes. Neuraminidase did not affect the modifying factor itself but did affect B27+ AS- lymphocytes such that they became unresponsive to modification. Sugar inhibition studies suggested that sugar groups are probably not involved in the function of the modifying factor. The availability of purified modifying factor should permit more detailed chemical analyses as well as functional studies to determine the significance of this molecule to the pathogenesis of ankylosing spondylitis.
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PMID:Biochemical studies on a factor isolated from Klebsiella K43-BTS1 that cross-reacts with cells from HLA-B27 positive patients with ankylosing spondylitis. 353 95


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