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Query: UNIPROT:P01889 (ankylosing spondylitis)
 5,717 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The aetiology of ankylosing spondylitis (AS) may involve certain enterobacteria. It is therefore interesting that serum polymeric IgA, a precursor of secretory IgA, was statistically elevated in active AS (n = 35) and that levels were comparable to those found in yersiniosis (n = 12); this might indicate antigenic stimulation by bacteria which are present in the intestines of AS patients. However, specific serum IgA to the incriminated enterobacteria Klebsiella, Shigella and Yersinia, as determined by ELISA, was not raised in the above AS patients. Nor were these titres raised in patients with idiopathic reactive arthritis (n = 21). In contrast, yersiniosis (n = 12) and shigellosis (n = 96) patients displayed marked increases in specific serum IgA titres to the respective infectants. It is proposed that AS may involve a set of enterobacteria rather than a few suspected species. Thus, despite the lack of raised group averages, screening of individual patients for specific IgA to several indicated bacteria might disclose whether or not raised serum IgA is related to enterobacterial activity. Apart from this, the above supports other reports indicating that serum IgA may be a useful parameter to assist in monitoring of disease activity in AS. Finally, it is suggested that study of a homogeneous group of reactive arthritis patients might facilitate aetiological research of seronegative arthropathies such as AS.
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PMID:Serum IgA to enterobacteria in ankylosing spondylitis. 354 Nov 70

The concentration of IgA and titre of IgA antibodies to several Gram-negative bacteria were measured in the serum and parotid saliva of patients with AS and normal tissue-typed individuals. Salivary IgA and antibody levels in the patients were identical with the control population. The serum antibody level against Yersinia enterocolica 0:3 was slightly raised in patients but there was no difference in the reactions to Klebsiella oxytoca strain MX100 or Escherichia coli 0111.B4. The serum IgA level was elevated in patients with AS, irrespective of HLA B27. We conclude that this approach is unlikely to provide convincing evidence of a link between Gram-negative bacteria and ankylosing spondylitis.
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PMID:IgA antibodies to gram-negative bacteria in the serum and saliva of patients with ankylosing spondylitis. 360 52

The paper is concerned with the results of a follow up of 67 patients with seronegative arthritis. The average duration of observation was 7.6 yrs. Diagnoses in 4 patients were established on a repeated clinicolaboratory and x-ray study: ankylosing spondylitis, Reiter's syndrome, Yersinia arthritis and gonorrheal arthritis. A picture of seropositive rheumatoid arthritis was noted in 16 patients (24%). In 47 patients arthritis remained seronegative. Of them in 30 patients a course of disease did not differ from that of seropositive rheumatoid arthritis. Considerable progression of disease was noted at the acute onset of disease with multiple involvement of the joints and a high inflammatory and immunological activity of a process. A morphological investigation of the synovial bioptates in 20 patients did not reveal a classical picture of rheumatoid synovitis even in a prolonged course of seronegative rheumatoid arthritis. The authors defined two variants of morphological changes in the synovial tissue in this group corresponding to a benign and progressive course of seronegative RA.
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PMID:[Evolution of seronegative arthritis]. 376 32

Reiter's syndrome can be induced by several different bacteria. A frequent cause in Finland is Yersinia enterocolitica serotypes 03 and 09, but these strains are rarely found in the United States. Although this does not exclude the possibility that U.S. patients with Reiter's syndrome have been infected with Yersinia, it is more likely that they develop Reiter's syndrome as a consequence of infection by non-Yersinia arthritis-causing organisms that share certain determinants with Yersinia organisms. We used radioimmunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis to analyze the serum antibodies against iodine 125-labeled, detergent-solubilized serotype 03 Y. enterocolitica. Our results demonstrated that most serum samples of United States subjects precipitate three to five radioactively labeled Yersinia molecules. A Yersinia antigen of 88K appeared to be of possible discriminatory value. Protein A-reacting antibodies directed against this antigen were detected in only two of twenty-five patients with rheumatoid arthritis and only seven of 44 normal control subjects, compared with 18 of 27 patients with Reiter's syndrome (p less than 0.005) and eight of 16 patients with ankylosing spondylitis (p less than 0.01). Our results indicate that, despite the relatively rare occurrence of Y. enterocolitica serotypes 03 and 09 infection in the United States, examination of the immune response to the serotype 03 Yersinia strain is a promising approach to the study of Reiter's syndrome in the United States.
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PMID:Antibodies against Yersinia enterocolitica in patients with Reiter's syndrome. 387 31

Lymphocyte transformation tests to Yersinia enterocolitica 0:3 and 0:6, Klebsiella pneumoniae and Streptococcus faecalis antigens have been carried out in ankylosing spondylitis, reactive arthritis/Reiter's disease and controls. Ankylosing spondylitis cases gave significantly lower responses than reactive arthritis/Reiter's to Yersinia enterocolitica 0:6 (p = 0.003) and Klebsiella pneumoniae (p = 0.008), and less than controls to S. faecalis (p = 0.008). It appears, therefore, that within the B27 arthritis population there is heterogeneity of cell-mediated response to certain enteric bacteria, with the hyporesponders manifesting ankylosing spondylitis and the hyper-responders reactive arthritis/Reiter's disease.
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PMID:Lymphocyte proliferative responses to bacterial antigens in B27-associated arthropathies. 391 98

The occurrence of IgM, IgG and IgA class Yersinia antibodies was studied at the beginning of an inflammatory joint disease and one year later in 354 adult patients using an ELISA technique. The control groups consisted of age and sex matched healthy persons living in the same geographical area as the patients, and of 64 patients with chronic rheumatoid arthritis. Yersinia antibodies of any Ig class were found in 9.0% of all the patients at the beginning of the disease, in 4.0% of the healthy controls and in 1.6% of the patients with chronic rheumatoid arthritis. Patients with ankylosing spondylitis, Reiter's disease or other reactive arthritis showed the highest prevalence (19.4%) of Yersinia antibodies, but in the whole material one half of the patients with Yersinia antibodies were clinically classified as rheumatoid or nonspecific arthritis. The elevated prevalence of Yersinia antibodies in patients with probable rheumatoid or nonspecific arthritis may indicate a reactive etiopathogenesis of arthritis also in some cases without previous evidence of gastrointestinal infection. Quantitation of IgG and IgA antibodies to Yersinia is important in the diagnosis of Yersinia arthritis. These antibodies may not be detected by the generally used agglutination test.
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PMID:Yersinia antibodies in inflammatory joint diseases. 633 56

Serum samples from patients with Reiter's syndrome, ankylosing spondylitis, Yersinia-induced arthritis and Yersinia infections not followed by arthritis were collected and assayed for complement-dependent cytotoxicity, using a standard dye-exclusion microcytotoxicity technique. A total of eighty-nine serum samples derived from these patients were compared to those of forty control subjects, using as target cells six different cultured cell line cells and peripheral blood mononuclear cells isolated from the blood samples of four subjects. Serum samples from only five of the subjects demonstrated cytotoxicity. This did not depend on whether the target cells were HLA-B27 or not. Hence, if antilymphocytic auto-antibodies are present in these patients, they will require a different technique for their detection.
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PMID:Absence of lymphotoxic antibodies in patients with Yersinia-induced arthritis, Reiter's syndrome and ankylosing spondylitis. 633 62

In ankylosing spondylitis (AS) and in yersinia arthritis the main findings in serum immunoglobulin (Ig) studies have been raised IgA in AS and a high anti-yersinia IgA and IgG response and the persistence of IgA class antibodies in yersinia arthritis. In order to study predisposition to high IgA response in AS and yersinia arthritis we measured the in-vitro Ig production in patients with AS and in persons who have once had yersinia arthritis, and we compared it with the Ig production in persons who have had yersiniosis but recovered without getting arthritis and with that in healthy controls. IgA secretion by peripheral blood lymphocytes stimulated by pokeweed mitogen was the same in all 4 groups, and no signs of higher IgA production in AS patients could be found. In AS patients lymphocyte activation by whole yersinia bacteria resulted in higher total IgG production than in healthy controls. The total number of plaque-forming cells in yersinia-stimulated cultures was significantly higher in persons who have had yersiniosis without arthritis than in persons who have suffered from yersinia arthritis or in persons in other groups. AS patients had low IgM production, which reverted to normal when hydrocortisone was added to the culture. The in-vitro Ig production in general did not correlate with the presence of the HLA B27 antigen but rather with the clinical history of the subjects studied.
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PMID:IgM, IgG, and IgA synthesis in vitro in persons suffering from yersinia arthritis and in patients with ankylosing spondylitis. 637 Jan 49

The frequency of attachment of postulated arthritogenic bacteria to lymphocytes from patients with ankylosing spondylitis (AS) and from healthy controls was examined using a fluorescent labelling technique. No significant differences in attachment frequency were seen with the arthritogenic or control bacterial strains between the patient and control groups using an "immediate" rosette assay. However, after overnight incubation at 37 degrees C, Klebsiella K43 and Escherichia coli bound significantly more frequently to lymphocytes when compared with rosettes examined without prior incubation. With this modified bacterial attachment test cells from patients with AS bound significantly more Klebsiella K43 and E. coli than did the cells from controls (2 p less than 0.05 and 2 p less than 0.001 respectively). No differences in binding were seen with Yersinia enterocolitica serotype 03. These results discount the idea of a specific receptor for arthritogenic bacteria being present on the surface of lymphocytes from AS patients.
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PMID:The binding to human lymphocytes of arthritogenic and non-arthritogenic bacteria. 639 61


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