Platelets and Bronchospasm

Page, C. P.; Paul, William; Morley, J.

doi:10.1159/000233571

Cited by 54 publications

(16 citation statements)

References 11 publications

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“…Furthermore, as platelet accumulation within the pulmonary vasculature and platelet activation have been reported to be associated with bronchoconstriction in clinical and experimental circumstances [24][25][26][27], our findings lead us to speculate on a possible involvement of platelets in asthmatic syndromes of nonimmunological origin.…”

Section: Antigen-specific Ige-dependent Platelet Activationmentioning

confidence: 67%

New Functions for Platelets and Their Pathological Implications

Capron¹,

Ameisen²,

Joseph³

et al. 1985

Int Arch Allergy Immunol

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We have recently demonstrated in Schistosoma mansoni infection that rat and human platelets could very efficiently kill parasite larvae, both in vivo and in vitro. The study of this IgE-dependent platelet effector function has led us to several subsequent findings. They concern: (1) the existence of a specific receptor for IgE on the platelet surface; (2) its close association with a platelet membrane glycoprotein of essential functional importance, the GPIIb-IIIa complex; (3) the observation, in extrinsic allergic asthma, of an allergen-specific IgE-dependent platelet activation; (4) the identification, in aspirin-sensitive asthma, of a similar, but non-IgE-dependent, platelet activation selectively induced by cyclo-oxygenase inhibitors, and prevented by salicylate. Beyond their implication in anti-parasite immunity, these findings provide a basis for new insights on the participation of platelets in disease.

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Section: Antigen-specific Ige-dependent Platelet Activationmentioning

confidence: 67%

New Functions for Platelets and Their Pathological Implications

Capron¹,

Ameisen²,

Joseph³

et al. 1985

Int Arch Allergy Immunol

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“…Haznedaroglu*, S. KirazlI*, Y. Baser + , S.V. Dündar* aa Platelets are considered to be pulmonary immune cells, because they possess many of the classical features of immune cells and participate in the pathogenesis of some pulmonary diseases [1][2][3]. These cells have been suggested to play a role in the evolution of inflammatory response against mycobacteria [4].…”

Section: In Vivo Platelet and T-lymphocyte Activities During Pulmonarmentioning

confidence: 99%

In vivo platelet and T-lymphocyte activities during pulmonary tuberculosis

Büyükaşık

Soylu²,

Soylu³

et al. 1998

Eur Respir J

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Platelets have been suggested to play a role in the inflammatory response, including defence against bacteria. The aims of this study were to determine in vivo platelet activity during the clinical course of pulmonary tuberculosis and to investigate whether or not there is a correlation between the magnitude of platelet activation and the extent of the pulmonary disease. T-lymphocyte activity was also analysed in the patients. Platelet factor-4 (PF4) and soluble interleukin-2 receptor-alpha (sIL-2Ralpha) concentrations were used as markers of platelet and T-lymphocyte activation, respectively. Twenty-five patients with pulmonary tuberculosis were studied. Fifteen healthy subjects served as a control group. The levels of both sIL-2Ralpha (3,000+/-1,948 pg x mL(-1)) and PF4 (103.1+/-6.7 IU x mL(-1)) were significantly higher in the patients with tuberculosis than in the control group (984+/-360 pg x mL(-1) and 78.2+/-23.9 IU x mL(-1), respectively) (Mann-Whitney U-test, p<0.001 for both comparisons). The plasma PF4 levels were found to be well correlated with the extent of pulmonary lesions on chest radiography (the Spearman's bivariate correlation analysis, r=0.65, p<0.001). However, sIL-2Ralpha concentrations did not correlate with the extent of disease. In conclusion, it has been suggested that platelet and T-lymphocyte activation occurs during pulmonary tuberculosis. The good correlation between platelet activation and the extent of pulmonary tuberculosis might be ascribed to a pathophysiological role of platelets in pulmonary tuberculosis.

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“…However, sim ultaneous measurement of changes in airway resist ance and sequestration of platelets within the pul monary vasculature revealed a dissociation between these two events. Thus in sensitised animals, low doses of allergen suffice to cause platelet accumula tion without detectable changes in airway resistance [36]. Conversely, during responses to intravenous in jection of PAF, increased airway resistance regularly preceded the pulmonary accumulation of platelets [36].…”

Section: Alternative Ige-dependent Determinant Of Late-onset Reactionsmentioning

confidence: 99%

“…It has long been appreciated that bronchoconstrictor responses may be induced by embolic stimuli; hence, it is reasonable to consider that such events may determine PAF-induced bronchospasm, since PAF causes transient retention of platelets within the pulmonary vasculature [36] and since anti-platelet an tisera inhibit responses to PAF [37,38]. However, sim ultaneous measurement of changes in airway resist ance and sequestration of platelets within the pul monary vasculature revealed a dissociation between these two events.…”

Section: Alternative Ige-dependent Determinant Of Late-onset Reactionsmentioning

confidence: 99%

Pharmacology of the Late Response to Allergen and Its Relevance to Asthma Prophylaxis

Morley¹,

Page²,

Sanjar³

1985

Int Arch Allergy Immunol

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Inhalation of allergen by sensitised asthmatics results in an acute increase of airways resistance that, in some individuals, is succeeded by a response of late-onset. Late-onset responses are associated with an increased airway reactivity to constrictor stimuli that lasts for several days and hence may be akin to exacerbation of clinical asthma. For this reason, much attention has been given to inhibition of late-onset reactions by glucocorticosteroids or by cromoglycate. Such effects have been cited as evidence of anti-asthma efficacy for these drugs and also for ketotifen, as might be anticipated from prophylactic efficacy in clinical asthma. More recently, a similar inhibitory effect has been demonstrated for theophylline, which is in marked contrast to Β-adrenoceptor agonists, which have long been known not to inhibit expression of late-onset reactions. The profile of drug sensitivity observed for late-onset reactions precludes mast cell stabilisation as an adequate explanation, since late-onset reactions are unaffected by Β-adrenoceptor agonists, notwithstanding the potency of such drugs as inhibitors of mast cell secretion; furthermore, late-onset reactions can be inhibited by nonste-roidal anti-inflammatory drugs, even though such drugs can enhance mast cell secretion. Rather, present evidence favours platelet-activating factor (PAF, Paf-acether, AGEPC) as a primary determinant of late-onset reactions, especially since responses to this material can be inhibited by cromoglycate, glucocorticosteroids, ketotifen and theophylline, and since there is substantial evidence that PAF has properties that could account for exacerbation of asthma.

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Platelets and Bronchospasm

Cited by 54 publications

References 11 publications

New Functions for Platelets and Their Pathological Implications

New Functions for Platelets and Their Pathological Implications

In vivo platelet and T-lymphocyte activities during pulmonary tuberculosis

Pharmacology of the Late Response to Allergen and Its Relevance to Asthma Prophylaxis

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