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Effects of a low extracellular magnesium concentration and endotoxin on IL-1beta and TNF-alpha release from, and mRNA levels in, isolated rat alveolar macrophages.
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2002
Year
Acute Lung InjuryTumour Necrosis FactorMrna LevelsInflammatory Lung DiseaseLung InflammationImmunologyCell DeathTnf-alpha ReleaseOxidative StressInflammationPulmonary PharmacologyCell SignalingMolecular PhysiologyAllergyChronic InflammationPharmacologyPhagocyteCytokineAnti-inflammatoryCalcium AntagonistMedicine
The aim of this study was to assess the effects of a low extracellular Mg2+ concentration and endotoxin on interleukin (IL)-1beta and tumour necrosis factor (TNF)-alpha release from, and mRNA levels in, rat alveolar macrophages. A low extracellular Mg2+ concentration enhanced the release of both cytokines, and this release was suppressed by a calcium antagonist, nifedipine. Bacterial lipopolysaccharide (LPS) also enhanced the release of both cytokines, and this enhancement was stronger in a low-Mg2+ medium than in control medium. Furthermore, LPS increased the mRNA levels of both cytokines in alveolar macrophages, and this increase was enhanced in low-Mg2+ medium. These results suggest that a low extracellular Mg2+ concentration and LPS stimulate the release of IL-1beta and TNF-alpha from rat alveolar macrophages by increasing the synthesis of both cytokines and by Ca2+ signaling pathways.