The possible role of gram-negative bacteria in the causation of seronegative spondyloarthropathies, and the response of polymorphs to gram-negative bacteria in ankylosing spondylitis, forms the basis of this study. Polymorph response to arthritogenic gram-negative bacteria in ankylosing spondylitis patients were examined by comparing them to HLA-B27 positive and negative healthy controls, and to a group of rheumatoid arthritis patients. Bacteria used in the assays had either a speculative or clear association with the seronegative spondyloarthropathies. Three different assays were used in this study to evaluate i) Polymorph motility ii) Polymorph chemiluminescence response to various stimuli and iii) Phagocytic ingestion of radio-labelled gram-negative bacteria. No difference was shown in motility between ankylosing spondylitis and normal polymorphs, although a culture filtrate of K. pneumoniae was shown to have some chemotactic quality. In addition phagocytic ingestion of enteric bacteria by polymorphs from ankylosing spondylitis patients was similar to normals. Therefore no abnormalities were shown in either the motility or phagocytic capacity of ankylosing spondylitis polymorphs. Initial studies using isolated polymorphs showed no difference in chemiluminescence response between patients and normal controls. A whole blood assay was then refined for use in this study, and chemiluminescence basal response was shown to be significantly increased in ankylosing spondylitis polymorphs compared to normal polymorphs. This indicated a pre-activation of normal polymorphs during the cell separation procedure, in our initial studies; thus concealing any inherent difference in chemiluminescence response between patient and normal polymorphs. Subsequent assays also showed a significantly enhanced chemiluminescence response in ankylosing spondylitis patients polymorphs compared to normals following stimulation with gram-negative bacteria and S. aureus. Contrastingly polymorphs from patients with rheumatoid arthritis showed an increase only to S. aureus. These results could indicate that gram-negative bacteria may contribute to an enhanced chemiluminescence response in ankylosing spondylitis patients, which is not specific. In addition, chemiluminescence response did not differ between HLA-B27 positive and negative normals, suggesting that enhanced activation develops with disease, rather than being inherent. Conclusions suggest a chronic activation and exposure of ankylosing spondylitis to gram-negative triggers.
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