Airway effects of purine nucleosides and nucleotides and release with bronchial provocation in asthma

Mann, J. S.; Holgate, S. T.; Renwick, A. G.; Cushley, M. J.

doi:10.1152/jappl.1986.61.5.1667

Cited by 154 publications

(95 citation statements)

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“…Although only an association was shown between adenosine and airway obstruction, not a direct causal relationship, previous studies have suggested that whatever is the source of adenosine in the airways, an increase in its level would potentiate the airway obstruction produced by other bronchoconstrictor stimuli [28,29].…”

Section: Discussionmentioning

confidence: 95%

Adenosine level in exhaled breath increases during exercise-induced bronchoconstriction

et al. 2005

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In asthmatic patients, airway obstruction provoked by exercise challenge is accompanied by an increase in plasma adenosine level. In this study, the current authors investigated if exercise-induced bronchoconstriction was associated with local changes of adenosine concentration in the airways.Oral exhaled breath condensate (EBC) collection (5-min duration) and forced expiratory volume in one second (FEV1) measurements were performed at rest (baseline) and 4-8 times after treadmill exercise challenge in healthy and asthmatic subjects. Adenosine concentration in EBC was determined by HPLC.Observations indicated that physical exercise results in bronchoconstriction together with a significant increase of adenosine level in EBC in asthmatic patients (mean¡SD maximal fall in FEV1 27¡13%; associated increase in adenosine 110¡76% as compared to baseline), but not in healthy control subjects. Exercise-induced changes in adenosine concentration correlated significantly with the fall in FEV1 values in asthmatic patients.In conclusion, the observed increase in adenosine concentration of oral exhaled breath condensate most probably reflects changes in the airways during exercise-induced bronchoconstriction. Due to its known bronchoconstrictor property in asthma, adenosine may contribute to the development of bronchospasm.

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Section: Discussionmentioning

confidence: 95%

Adenosine level in exhaled breath increases during exercise-induced bronchoconstriction

et al. 2005

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“…Adenosine has long been thought to play a role in the pathogenesis of allergic airway disease and asthma (9,13,30,45). However, the mechanisms of adenosinemediated lung damage are poorly understood.…”

Section: Discussionmentioning

confidence: 99%

Gene expression profiling in inflammatory airway disease associated with elevated adenosine

Banerjee

Young

Volmer

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Adenosine has been implicated as a modulator of inflammatory processes central to asthma. However, the molecular mechanisms involved are poorly understood. We used Atlas mouse cDNA arrays to analyze differential gene expression in association with lung inflammation resulting from elevated adenosine in adenosine deaminase (ADA)-deficient mice. We report that of the 1,176 genes on the array, the expression patterns of 280 genes were consistently altered. Of these genes, the steady-state levels of 93 genes were upregulated and 29 were downregulated. We also show that lowering adenosine levels with ADA enzyme therapy has striking effects on gene expression that may be associated with resolution of pulmonary eosinophilia. In addition, we confirmed the nucleic acid and protein expression of vascular endothelial growth factor and monocyte chemoattractant protein-3, two candidate genes that may be regulated by adenosine. In conclusion, high-throughput profiling of gene expression by cDNA array hybridization has provided an overview of critical regulatory genes involved in airway inflammation in ADA-deficient mice. These mice will serve as a useful in vivo model for characterizing molecular mechanisms of adenosine-mediated lung damage.

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“…These pathways are activated by extracellular purines, which include adenosine triphosphate (ATP) and its metabolites adenosine diphosphate, adenosine monophosphate (AMP), and adenosine. Adenosine, in particular, has been linked to infl ammatory airways diseases, 1 including twofold to fourfold elevations in blood 2,3 and BAL fl uid 4 of subjects with asthma. Similarly, adenosine concentrations in exhaled breath condensate (EBC) are elevated in subjects with stable asthma, 5,6 increased with asthma exacerbations, 7 and decreased with successful treatment.…”

Section: Original Research Obstructive Lung Diseasesmentioning

confidence: 99%

Elevated Airway Purines in COPD

Esther

Lazaar

Bordonali

et al. 2011

Chest

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Purinergic signaling pathways regulate airways defense mechanisms, including mucociliary clearance and infl ammatory responses. These pathways are activated by extracellular purines, which include adenosine triphosphate (ATP) and its metabolites adenosine diphosphate, adenosine monophosphate (AMP), and adenosine. Adenosine, in particular, has been linked to infl ammatory airways diseases, 1 including twofold to fourfold elevations in blood 2,3 and BAL fl uid 4 of subjects with asthma. Similarly, adenosine concentrations in exhaled breath condensate (EBC) are elevated in subjects with stable asthma, 5,6 increased with asthma exacerbations, 7 and decreased with successful treatment. Findings from animal models, particularly the adenosine deaminase knockout mouse, 8,9 further support a link between airway infl ammation and lung adenosine.These data suggest that purinergic signaling pathways may be active in infl ammatory lung diseases such as COPD and may be targets for therapeutic intervention. 10 Indeed, elevated airway adenosine concentrations in COPD have been inferred from studies of human airway adenosine receptors, 11 and several reviews have touted potential benefi ts of pharmacologic blockade of adenosine receptors. 10,12 Although these benefi ts are a reasonable extrapolation from the animal 8,13 and human studies, 4,5 a recent investigation suggested that airway adenosine concentrations (as measured in sputum) may actually be lower in COPD. 14 However, adenosine concentrations in respiratory samples such as sputum or BAL can be altered unpredictably by extracellular metabolism during processing or by mechanical and osmotic forces that trigger purine release during collection.

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Airway effects of purine nucleosides and nucleotides and release with bronchial provocation in asthma

Cited by 154 publications

References 0 publications

Adenosine level in exhaled breath increases during exercise-induced bronchoconstriction

Adenosine level in exhaled breath increases during exercise-induced bronchoconstriction

Gene expression profiling in inflammatory airway disease associated with elevated adenosine

Elevated Airway Purines in COPD

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