STIMULATION OF WHOLE-BLOOD CULTURES IN PATIENTS WITH ANKYLOSING-SPONDYLITIS BY A MITOGEN DERIVED FROM MYCOPLASMA-ARTHRITIDIS (MAS) AND OTHER MITOGENS

Citation
Jm. Brand et al., STIMULATION OF WHOLE-BLOOD CULTURES IN PATIENTS WITH ANKYLOSING-SPONDYLITIS BY A MITOGEN DERIVED FROM MYCOPLASMA-ARTHRITIDIS (MAS) AND OTHER MITOGENS, Rheumatology international, 16(5), 1997, pp. 207-211
Citations number
33
Categorie Soggetti
Rheumatology
Journal title
ISSN journal
01728172
Volume
16
Issue
5
Year of publication
1997
Pages
207 - 211
Database
ISI
SICI code
0172-8172(1997)16:5<207:SOWCIP>2.0.ZU;2-T
Abstract
In this study we compared cytokine production and cell proliferation o f immunocompetent cells derived from patients with ankylosing spondyli tis (AS) to those from healthy blood donors using a whole blood assay. To this end, blood cell cultures were stimulated with the superantige ns MAS (Mycoplasma arthritidis supernatant) and staphylococcal enterot oxin B (SEE) and the plant lectins phytohaemagglutinin (PHA) and conca navalin A (Con A). The number of white blood cells (WBC) and lymphocyt e subsets were also determined. Cell proliferation and levels of inter feron-gamma (IFN-gamma), interleukin-lp (IL-1 beta) and interleukin-6 (IL-6) were measured after stimulation with the different mitogens. An ELISA test was used to analyse supernatant cytokine levels. Individua ls with AS showed significantly lower IFN-gamma concentrations and mar kedly lower cell proliferation rates with all tested mitogens than hea lthy controls, while there was no significant difference in IL-6 synth esis. IL-1 beta levels were slightly impaired in the patient group, bu t only blood cell cultures stimulates with MAS showed a statistical si gnificance. Furthermore, there was a significant elevation of leucocyt es and lymphocytes in patients with AS resulting in higher numbers of CD4-positive cells, which implies a higher CD4:CD8 cell ratio. CD19- a nd CD8-positive cells were not significantly distinct compared to heal thy controls. This deviation in cytokine levels and cell proliferation points to a suppression of T lymphocytes. A disturbed T-lymphocyte fu nction may play a part in the pathogenesis of AS.