Effect of sulphasalazine and sulphapyridine on neutrophil superoxide production: role of cytosolic free calcium
Article Abstract:
Rheumatoid arthritis (RA) is a disease causing inflammation of the joints, stiffness, swelling, overgrowth of cartilage tissue, and pain. Neutrophils, a type of white blood cell involved in the inflammatory process of RA, release factors such as highly reactive oxygen radicals that cause tissue destruction and abnormal immune reactions. The drug sulphasalazine is effective in treating RA, although its mechanism of action is not clear. The effects of sulphasalazine and its metabolite, sulphapyridine, on the production of superoxide, a type of oxygen radical in neutrophils, was examined. The synthetic substance N-formyl-methionyl-leucyl-phenylalanine (fMLP) and calcium ionophore A23187, which increases the movement of calcium across cell membranes, activate the production of superoxide by neutrophils. The fMLP binds to a specific site on the neutrophil membrane called a receptor to exert its effects. Superoxide production activated by fMLP and A23187 is accompanied by an increase in the intracellular levels of calcium. Both sulphasalazine and sulphapyridine prevent the intracellular rise in calcium levels and the production of superoxide by neutrophils activated by fMLP and A23187. However, sulphasalazine and sulphapyridine did not prevent superoxide production by the ester phorbol myristate acetate, which is not associated with a rise in intracellular calcium levels. Thus, the anti-rheumatic effects of sulphasalazine may be caused by the prevention of superoxide production, which is accompanied by a rise in intracellular calcium. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1990
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Evidence for differential effects of sulphasalazine on systemic and mucosal immunity in rheumatoid arthritis
Article Abstract:
In rheumatoid arthritis (RA) patients, sulphasalazine appears to inhibit the production of immunoglobulins generated in bone marrow, spleen, and lymph nodes without affecting immunoglobulins produced by mucosal tissues such as the lining of the mouth and intestines. Blood was drawn, saliva collected, and fluid from the small intestine was collected during biopsy from 21 RA patients before sulphasalazine treatment and 16 weeks after therapy. Samples were analyzed for levels of immunoglobulins types G, A, and M; antibodies against gluten, an allergen found in wheat and other foods; rheumatoid factors; and interleukin-6, a mediator of inflammation. Immunoglobulin levels in saliva and intestinal fluid were unchanged while blood levels of all immunologic factors measured declined. It seems likely that sulphasalazine suppresses the production of immunoglobulins by B cells, probably by affecting production of interleukin-6, which stimulates production of these factors.
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1995
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Signalling through neutrophil FcgammaRIII, FcgammaRII, and CD59 is not impaired in active rheumatoid arthritis
Article Abstract:
Neutrophils from patients with rheumatoid arthritis (RA) appear to function normally in response to selected immune system compounds. Neutrophils are white blood cells that destroy and remove bacteria, debris, and solid particles from the blood. Researchers compared the calcium production levels of neutrophils from 8 patients with RA and 8 healthy blood donors (the control group) in response to the antibodies CD16, CD32, and CD59 and followed by a second cross-linking antibody. There was no difference in calcium production between the neutrophils from the RA patients and the control samples in response to any of the antibodies when followed by the cross-linking antibody. However, neutrophils from the RA patients produced more calcium than the control samples when stimulated by CD16 and not followed by the addition of the cross-linking antibody.
Publication Name: Annals of the Rheumatic Diseases
Subject: Health
ISSN: 0003-4967
Year: 1996
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