Abstract
We have compared superoxide (O2-) production from cytokine-treated rheumatoid arthritis (RA) vs. control neutrophils (PMN). Exposure of adherent peripheral blood PMN to cytokines known to be present in RA joints (IL-1 beta, TNF-alpha, GM-CSF) resulted in enhanced O2- production from both RA and controls. With few exceptions, we did not find significant differences in enhanced O2- production, between RA and controls. By enhancing O2- production from PMN adherent to articular cartilage, cytokines may influence the potential for joint damage in RA.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Aged
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Arthritis, Rheumatoid / blood*
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Cytochrome c Group / blood
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Cytokines / pharmacology*
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Female
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Granulocyte-Macrophage Colony-Stimulating Factor / pharmacology
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Humans
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Interleukin-1 / pharmacology
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Male
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Middle Aged
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N-Formylmethionine Leucyl-Phenylalanine / pharmacology
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Neutrophils / metabolism*
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Superoxides / blood*
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Tumor Necrosis Factor-alpha / pharmacology
Substances
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Cytochrome c Group
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Cytokines
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Interleukin-1
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Tumor Necrosis Factor-alpha
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Superoxides
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N-Formylmethionine Leucyl-Phenylalanine
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Granulocyte-Macrophage Colony-Stimulating Factor