PubMed · 169723
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J W Hadden. 1975-06-13. Cyclic nucleotides in lymphocyte function.. https://doi.org/10.1111/j.1749-6632.1975.tb36062.x
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The drugs used in asthmatic attacks must act on the two major mechanisms of the disease: bronchial obstruction and inflammation of the airways. Two main classes of drugs are available to reach these targets: bronchodilators, headed by beta 2-stimulants, and anti-inflammatory drugs of the corticosteroid family. Bronchodilatation obtained with beta 2-stimulants is the first and most effective treatment of the attack. These drugs are usually administered by inhalation: metered-dose aerosols with or without inhalation chambers, or nebulization for severe attacks. Very high doses can be used without fear of side-effects, the principal objective of this treatment being to relieve bronchial obstruction. In the absence of rapid and lasting improvement bronchodilators must always be combined with corticosteroids. In all cases medical supervision immediately after the attacks is necessary and the patient should subsequently be put under care of pneumologists.
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Interactions between interleukin 8 (IL-8) and endothelial cells play an important role in the emigration of mononuclear cells from the blood into areas of inflammation. We examined the ability of specific second-line antirheumatic drugs to regulate (IL-8) gene expression and protein secretion in interleukin 1 (IL-1) stimulated human umbilical vein endothelial cells and peripheral blood mononuclear cells. The drugs sodium aurothiomalate, D-penicillamine and sulphasalazine were all able to modulate IL-8 mRNA synthesis in and protein secretion from endothelial cells. A bimodal effect was observed: at low concentrations IL-8 was suppressed, whereas higher concentrations resulted in an increased IL-8 production. In endothelial cells, treatment with hydrocortisone led to a linear suppression of IL-8 production in concentrations ranging from 0.5 micrograms/ml up to 500 micrograms/ml. Sulphapyridine, auranofin, hydroxychloroquine and methotrexate, had no effect on IL-8 secretion in endothelial cells. By contrast, 5-aminosalicylic acid induced a threefold increase in the IL-8 release. In peripheral blood mononuclear cells it was only possible to suppress the IL-8 production by hydrocortisone treatment. These results indicate that suppression of IL-8 production in endothelial cells could be an important factor in the mode of action for a number of second-line antirheumatic drugs.