Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: KEGG:D00527 (Nedocromil sodium)
 190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We conducted a series of studies investigating the antiinflammatory effects of nedocromil sodium, with particular reference to its effects on human bronchial epithelial cells and eosinophils in vitro and on eosinophils in vivo. Nedocromil sodium produced a dose-related inhibition of ozone-induced IL-8 release from human bronchial epithelial cells and also attenuated the release of granulocyte macrophage colony-stimulating factor, tumor necrosis factor-alpha, and soluble intercellular adhesion molecule 1. The culture medium from human bronchial epithelial cell cultures, containing the proinflammatory cytokines IL-8, granulocyte macrophage colony-stimulating factor, "regulated on activation, normal T expressed and secreted," IL-1 beta, and tumor necrosis factor-alpha, increased eosinophil chemotaxis and eosinophil adhesion to cultured human endothelial cells. The chemotaxis and increased adhesion were blocked in the presence of nedocromil sodium. The drug also abrogated the epithelial cell dysfunction (assessed as ciliary beat frequency) induced by the presence of activated eosinophils and blocked the release of eosinophil cationic protein from the eosinophils. We also conducted a double-blind placebo-controlled study of the effects of regular albuterol 200 micrograms or nedocromil sodium 4 mg, both given four times daily for 16 weeks, on inflammatory cell numbers in bronchial biopsy and bronchoalveolar lavage samples. Assessed in terms of total and activated eosinophils in biopsy samples, inflammation decreased with nedocromil sodium and was significantly different from a deterioration with albuterol, although neither of these changes was significantly different from that with placebo treatment. Levels of eosinophil cationic protein in bronchoalveolar lavage samples showed a similar trend.
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PMID:Nedocromil sodium and airway inflammation in vivo and in vitro. 893 77

Nasal epithelial cells maintain eosinophil survival by secreting granulocyte/macrophage colony-stimulating factor (GM-CSF). Corticosteroids antagonize eosinophil viability induced by GM-CSF. We investigated the effect of topical corticosteroids and nedocromil sodium on the release of GM-CSF from nasal polyp epithelial cells. Epithelial cells were obtained from 19 patients undergoing nasal polypectomy and cultured. After reaching confluence, cultured cells were stimulated with 10% foetal calf serum in the absence and presence of four topical corticosteroids and nedocromil sodium for 48 h. GM-CSF was measured by enzyme linked immunosorbent assay (ELISA). Fluticasone propionate was the most potent inhibitor of GM-CSF release (IC25 = 46 pM) closely followed by budesonide (IC25 = 4 nM), beclomethasone dipropionate (IC25 = 40 nM) and triamcinolone acetonide (IC25 = 75 nM). Nedocromil sodium had no effect on GM-CSF release. We conclude that the effect of topical steroids on reducing eosinophil infiltration in nasal polyps may be due in part to downregulation, among other cytokines, of epithelial GM-CSF production which prolongs eosinophil viability. Quantitatively, fluticasone propionate inhibited GM-CSF production more potently than budesonide, beclomethasone dipropionate and triamcinolone acetonide.
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PMID:Inhibition of GM-CSF secretion by topical corticosteroids and nedocromil sodium. A comparison study using nasal polyp epithelial cells. 1086 4