Effect of klebsiella capsular antisera on lymphocytes from patients with ankylosing spondylitis

Cross‐reactivity between antibodies to 2 strains of Klebsiella pneumoniae (K43 and F77) and the peripheral blood lymphocytes of patients with ankylosing spondylitis (AS) was examined in 3 separate antibody binding and cytotoxicity assays. Using K pneumoniae antisera in a chromium release cytotoxicity assay, we found no difference in the reactions of cells from AS patients and those from control subjects. This result contrasts with the results of previous studies. Similarly, using an enzyme‐linked immunosorbent assay, we detected no significant increase in antibody binding to peripheral blood mononuclear cells (PBMC) in HLA–B27 positive patients with AS. Low levels of antibody binding were detected by a fluoresceinated antibody binding assay; however, normal rabbit serum, which was used as a control, was shown to have a binding affinity for PBMC that was significantly greater than that of specific K pneumoniae antisera. The results of our present study do not support the concept of a specific cross‐reactivity between antibodies to K pneumoniae and the PBMC of patients with AS who are HLA–B27 positive.

Section: Discussionsupporting

confidence: 79%

Failure Of klebsiella pneumoniae antibodies to cross‐react with peripheral blood mononuclear cells from patients with ankylosing spondylitis

Cameron

Russell

Easter

et al. 1987

“…The course of the illness was monitored using the following clinical parameters: duration of morning stiffness; number of swollen or painful joints, with the exclusion of hip joints; assessment of back pain and general condition, using The patients were observed at the outpatient department 3, 8,16, and 26 weeks after the start of treatment. The change from baseline at week 26 was computed as the posttreatment score minus the baseline score.…”

mentioning

confidence: 99%

Sulfasalazine in the treatment of ankylosing spondylitis

Nissilä

Lehtinen

Leirisalo‐Repo

et al. 1988

113

Eighty-five patients with active ankylosing spondylitis (AS) were randomized to receive either sulfasalazine ( 5 3 gm/day, mean 2.5) or placebo for 26 weeks. There was a statistically significant improvement, compared with baseline, in most of the clinical variables in patients receiving the active drug. Laboratory parameters (erythrocyte sedimentation rate, Creactive protein, IgG, IgM, and IgA) also improved during the active treatment, suggesting a beneficial effect of sulfasalazine on AS. At the end of the treatment, significant differences between the sulfasalazine and placebo groups were observed in morning stiffness, chest expansion, erythrocyte sedimentation rate, and in all immunoglobulin classes. Two patients in each treatment group discontinued the trial because of side effects. Enteric-coated sulfasalazine seemed to be effective and well tolerated in patients with active AS.Ankylosing spondylitis (AS) is one of the HLA-B27-associated diseases (1). In some of these diseases, infection is considered to be an etiologic factor.To date, however, the role of infection in the etiology of AS has not been confirmed. The association beFrom the Rheumatism Foundation

Anti‐HLA–B27 antibodies in sera from patients with gram‐negative bacterial infections

Cavender

Ziff

1986

Several forms of seronegative polyarthritis are strongly associated with HLA-B27, and a number of micramorganisms have been implicated in the etiology of these diseases. To explain the association between HLA--B27 and arthritis initiated by infection with these organisms, it has been proposed that there is immunologic cross-reactivity between the B27 molecule and 1 or more microbial antigens, and that this cross-reactivity leads to tolerance to such infection andlor to the production of anti-HLA-B27 cross-reactive antibodies. Such cross-reactive antibodies were detected in the sera of only 2 of 63 patients recently infected with Shigella JEexneri, Campylobacter jejuni, or Yersinia enterocolitica who hiad highly significant antibody levels against the infecting bacterial species. Most striking was the absence caf anti-HLA-B27 antibody in the serum of 16 of 17 patients who developed reactive arthritis following Yersinia infection.