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• W2168162287 abstract "Cytokines, including TNFα and IL-1β, are central to the chronic inflammatory process and tissue damage that characterises diseases such as rheumatoid arthritis. The mechanisms responsible for long-term generation of these molecules are poorly understood. We have previously demonstrated impaired activity of Na,K-ATPase, a key enzyme regulating intracellular cation levels, on rheumatoid mononuclear cells. Mimicking this `defect' on normal mononuclear cells with ouabain has been shown to induce TNFα and, in particular, IL-1β production, whereas IL-6 synthesis was suppressed. A similar pattern of cytokine generation was noted when mononuclear cells were treated with the sodium ionophore, monensin. Induction of cytokine production was related to up-regulation of the appropriate mRNA, although enhanced secretion of processed IL-1β was also observed. The mechanism underlying these cellular responses appears to involve sodium/calcium exchange across the cell membrane. Impaired Na,K-ATPase activity might promote pro-inflammatory cytokine secretion in patients with rheumatoid arthritis." @default.
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• W2168162287 date "1997-01-01" @default.
• W2168162287 modified "2023-09-26" @default.
• W2168162287 title "Modulation of cytokine production by human mononuclear cells following impairment of Na,K-ATPase activity" @default.
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• W2168162287 doi "https://doi.org/10.1016/s0167-4889(96)00116-4" @default.
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