Inhibition of Human Eosinophil Chemotaxis and of the IgE-Dependent Stimulation of Human Blood Platelets by Cetirizine

C, De Vos; Joseph, M.; Leprevost, Corinne; Vorng, Han; Tomassini, Margherita; Capron, M; Caprón, A

doi:10.1159/000234789

Cited by 67 publications

(22 citation statements)

References 11 publications

(18 reference statements)

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“…Evidence of a pathogenic role of eosinophils in allergic rhinitis has been well established [9,10]. Recently, it has been reported that terfenadine, an antihistamine, inhibited the secretion of IL-5 in human peripheral blood mononuclear cells [11] and that cetirizine, another antihistamine, was reported to inhibit eosinophil chemotaxis in vitro [12]. Therefore, it is suggested that antihistamines possess anti-inflammatory activity to inhibit eosinophil chemotaxis in the nasal mucosa by inhibiting the gene expression of IL-5, in addition to their histamine-blocking effect at H1R.…”

Section: Discussionmentioning

confidence: 99%

Preseasonal prophylactic treatment with antihistamines suppresses IL−5 but not IL-33 mRNA expression in the nasal mucosa of patients with seasonal allergic rhinitis caused by Japanese cedar pollen

Kitamura¹,

Mizuguchi

Ogishi

et al. 2012

Acta Oto-Laryngologica

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Section: Discussionmentioning

confidence: 99%

Preseasonal prophylactic treatment with antihistamines suppresses IL−5 but not IL-33 mRNA expression in the nasal mucosa of patients with seasonal allergic rhinitis caused by Japanese cedar pollen

Kitamura¹,

Mizuguchi

Ogishi

et al. 2012

Acta Oto-Laryngologica

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“…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%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

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An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

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“…In addition to its anti-H1-receptor properties, cetirizine possesses inhibitory properties for basophils [511], and eosinophils [512][513][514]. For instance, cetirizine has been shown to inhibit chemotaxis of eosinophils in vivo [512,513,515], and in vitro [514], reduces both PAF-induced receptor complement expression and cytotoxicity [516], prevents IL-5-induced ICAM-1 expression in vitro [517], and selectively blocks adhesion of eosinophil to endothelial cells [518] possibly via the very late activation antigen-4 (VLA-4)/vascular cell adhesion molecule-1 (VCAM-1) interaction.…”

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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Inhibition of Human Eosinophil Chemotaxis and of the IgE-Dependent Stimulation of Human Blood Platelets by Cetirizine

Cited by 67 publications

References 11 publications

Preseasonal prophylactic treatment with antihistamines suppresses IL−5 but not IL-33 mRNA expression in the nasal mucosa of patients with seasonal allergic rhinitis caused by Japanese cedar pollen

Preseasonal prophylactic treatment with antihistamines suppresses IL−5 but not IL-33 mRNA expression in the nasal mucosa of patients with seasonal allergic rhinitis caused by Japanese cedar pollen

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

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

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