1992
DOI: 10.1016/0091-6749(92)90222-n
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The effect of sodium cromoglycate on platelets: An in vivo and in vitro approach

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Cited by 9 publications
(7 citation statements)
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“…On the other hand, it has recently been demonstrated that monomeric IgE could stimulate signalling pathways in mast cells leading to an important cytokine production including interleukin (IL)‐4, tumour necrosis factor (TNF)‐α, IL‐13, and IL‐6. An effect of monomeric IgE has previously been observed in other inflammatory cells (36,37) and may provide an explanation for the effect of IgE rich serum on human isolated airways.…”
Section: Discussionmentioning
confidence: 54%
“…On the other hand, it has recently been demonstrated that monomeric IgE could stimulate signalling pathways in mast cells leading to an important cytokine production including interleukin (IL)‐4, tumour necrosis factor (TNF)‐α, IL‐13, and IL‐6. An effect of monomeric IgE has previously been observed in other inflammatory cells (36,37) and may provide an explanation for the effect of IgE rich serum on human isolated airways.…”
Section: Discussionmentioning
confidence: 54%
“…2,3 Furthermore, drugs that could inhibit this platelet activation induced by inflammatory stimuli or allergen, such as the antiallergic agents nedocromil sodium, disodium cromoglycate, and cetirizine, did not inhibit platelet aggregation. 68,69 We have very recently confirmed this hypothesis by demonstrating that when using ADP as a stimulus for platelet activation, there are distinct signaling mechanisms involved in platelet aggregation and platelet chemotaxis (Amison, unpublished observation). 38 In particular, we have demonstrated that P2Y 1 receptors for ADP, signaling through RhoA, are required for the activation of platelets by inflammatory stimuli, whereas P2Y 12 receptors that are required for platelet aggregation have no such effects.…”
Section: Dichotomy Of Platelet Activation and Future Perspectives Formentioning
confidence: 62%
“…This accelerated platelet consumption correlates to a shortened time taken to regenerate the platelet population. These phenomena can be corrected by treatment of asthmatic patients with glucocorticoids, or platelets treated with di-sodium chromoglycate in vitro before re-infusion, although these anti-inflammatory drugs have no known direct affects on platelet activation (Taytard et al, 1985;Tunon-De-Lara et al, 1992).…”
Section: Platelet Activation In Asthma and Rhinitismentioning
confidence: 99%
“…The process of platelet activation by IgE has been demonstrated to be inhibited by drugs used for the treatment of atopic asthma and allergies, such as nedocromil sodium, disodium cromoglycate and cetirizine (Thorel et al, 1988;Tsicopoulos et al, 1988;De Vos et al, 1989;Joseph et al, 1989Joseph et al, , 1993Tunon-De-Lara et al, 1992). IgE stimulation of platelets represents a non-thrombotic pathway by which platelets can be specifically activated by allergen, and thus directly contribute to the inflammatory responses observed in allergy.…”
Section: Platelet Involvement In Antigen Recognitionmentioning
confidence: 99%