Effects of sodium cromoglycate and nedocromil sodium on histamine secretion from human lung mast cells.

Leung, K. B. P.; Flint, K. C.; Brostoff, Jonathan; Hudspith, B N; Johnson, N M; Lau, H. Y. A.; Liu, W. L.; Pearce, F. L.

doi:10.1136/thx.43.10.756

Cited by 121 publications

(62 citation statements)

References 12 publications

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“…Although several investigators have demonstrated that nedocromil sodium can inhibit the activation of different inflammatory cell types, including mast cells, eosinophils, monocytes, macrophages and platelets in vitro [23][24][25][26][27], the precise mode of action of this drug has only recently become clear. Studies have demonstrated that both sodium cromoglycate [28] and nedocromil sodium [29] block a chloride ion channel in rat basophil leukaemia cells, and have suggested that inhibition of this or a similar channel may inhibit mast cell activation, since influx of chloride ions into the mast cell is in part a prerequisite for calcium influx [30] and subsequent activation of this cell type.…”

Section: Discussionmentioning

confidence: 99%

Ozone-induced mediator release from human bronchial epithelial cells in vitro and the influence of nedocromil sodium

Rusznák¹,

Devalia²,

Sapsford³

et al. 1996

Eur Respir J

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Section: Discussionmentioning

confidence: 99%

Ozone-induced mediator release from human bronchial epithelial cells in vitro and the influence of nedocromil sodium

Rusznák¹,

Devalia²,

Sapsford³

et al. 1996

Eur Respir J

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“…Nedocromil sodium is a pyranoquinoline dicarboxyline acid which has been demonstrated to have some beneficial effects in various models of asthma, including human airway response to hyperosmolar challenge [488], PAF-mediated bronchoconstriction [489], early and late responses to allergen challenge in asthmatics [490,491], and eosinophil recruitment in humans [491]. Besides its inhibitory action on mast cells, neutrophils, monocytes and platelets [492][493][494][495][496], nedocromil sodium has been shown to block various eosinophil functions, including secretion of granule proteins [497], eosinophil chemotaxis [498,499], surface antigen expression [500], leukotriene C 4 secretion in response to various agents [499,501] as well as density change, damage to airway epithelium [502,503] and other cytotoxic mechanisms [498,500]. Hence, these inhibitory effects of nedocromil on eosinophil function suggest that it may be effective in eosinophil-related disease, such as asthma.…”

Section: Xanthines and Selective Phosphodiesterase Inhibitorsmentioning

confidence: 99%

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part II)

Kroegel¹,

Warner²,

Jc³

et al. 1994

Eur Respir J

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The second part of this review on eosinophils focuses on biological cell functions and surveys the various deleterious mechanisms involved in the eosinophil-dominated inflammatory reaction. It discusses the possible pathogenic role of eosinophils in several eosinophil-related diseases, such as parasitic infections, interstitial lung disorders and bronchial diseases, graft rejection, vasculitic granulomatous disorders, pleural effusion, and bronchogenic tumours.The final section of the article highlights the possible recent pharmacological and future therapeutic approaches in modifying eosinophil recruitment and function. Eur Respir J., 1994, 7, 743-760 This paper is published as a follow-on to "Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part I)"* (Eur Respir J, 1994; 7: 519-543). Biological cell functionsThe eosinophil mediates its effector functions through various distinct cellular mechanisms, namely nonoxidative, oxidative, and humoral mechanisms ( fig. 7). Nonoxidative mechanismsAs mentioned previously, the three basic proteins as well as eosinophil peroxidase (EPO) have toxic properties independent of molecular oxygen species. For instance, major basic protein (MBP) [323], eosinophil cationic protein (ECP) [324] and EPO in the presence of hydrogen superoxide and a halide [99] kill helminthic parasites in vitro. In addition, these proteins are toxic for tumour cells and/or mammalian cells [325], including human pulmonary parenchyma and interstitial matrix [326,327], cultured human lung epithelial cells [328], and guinea-pig respiratory epithelium [252, 253,329]. Furthermore, it has been demonstrated that MBP damages human bronchial epithelium, which consists of desquamation and destruction of ciliated cells [329]. Finally, release of their granule proteins by plateletactivating factor (PAF)-activated intact eosinophils has been shown to imitate the characteristic pathological findings of airway epithelium in asthma [330].In addition to their cytotoxic action, eosinophil cationic proteins at certain subtoxic concentrations also stimulate other inflammatory cells. For instance, MBP and ECP have been shown to degranulate platelets [305], induce histamine release from mast cells and basophils [240, 245,331], as well as superoxide anion generation and lysosomal enzyme release by human neutrophils [264].Finally, eosinophil proteins may affect airway muscle function and hyperresponsiveness. Recent reports investigating the effects of direct intratracheal instillation of purified eosinophil granule proteins on pulmonary function and airway responsiveness in primates [281,332] have shown that MBP induces a dose-related increase in airway responsiveness to inhaled methacholine. In the same model, both MBP and EPO caused a transient bronchoconstriction immediately after instillation, that resolved within 1 h. Interestingly, other eosinophil granular proteins failed to effect airway responsiveness or pulmonary function.Mode of action. The mode of action of these basic proteins is n...

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“…during MBS airway challenge, we examined the effects of nedocromil sodium and of frusemide which are both able to inhibit the release of histamine or leukotrienes from inflammatory cells (Leung et al, 1988;Bruinjzeel et al, 1989;Anderson et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Effect of sodium metabisulphite on bronchial blood flow in conscious sheep: pharmacological modulation

Nichol

Parsons

Chung³

1994

British J Pharmacology

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1 Sodium metabisulphite (MBS) can induce bronchoconstriction in patients with asthma. We investigated the effects of MBS aerosol on bronchial blood velocity (Vbr) and pulmonary resistance in intubated conscious sheep. 2 Bronchial blood velocity was measured by implanting a 20 MHz ultrasonic Doppler flow probe on the common bronchial branch of the bronchoesophageal artery. 3 Inhaled MBS induced a dose-dependent, transient increase in Vb. lasting for a few minutes without any changes in aortic and pulmonary artery pressures. There was some tachyphylaxis of the Vbr response to successive inhalations of MBS. 4 The cholinoceptor antagonist, ipratropium bromide and the H, and H2 histamine antagonists, chlorpheniramine and cimetidine, had no significant effect on MBS-induced increase on Vbr. The loop diuretic, frusemide, and the anti-inflammatory drug, nedocromil sodium, which both inhibit MBSinduced bronchoconstriction in patients with asthma, were, also without effect. 5 We conclude that MBS induces bronchial vasodilatation in conscious sheep, and that this effect is not dependent on the release of histamine or other mediators, or an activation of cholinergic pathways.

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Effects of sodium cromoglycate and nedocromil sodium on histamine secretion from human lung mast cells.

Cited by 121 publications

References 12 publications

Ozone-induced mediator release from human bronchial epithelial cells in vitro and the influence of nedocromil sodium

Ozone-induced mediator release from human bronchial epithelial cells in vitro and the influence of nedocromil sodium

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part II)

Effect of sodium metabisulphite on bronchial blood flow in conscious sheep: pharmacological modulation

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