Extracellular adenosine triphosphate and chronic obstructive pulmonary disease
Marek Lommatzsch1, Sanja Cicko, Tobias Müller
1Department of Pneumology, University of Rostock, Rostock, Germany.
American Journal of Respiratory and Critical Care Medicine
|January 23, 2010
Summary
Extracellular ATP (adenosine triphosphate) is elevated in the airways of chronic obstructive pulmonary disease (COPD) patients, contributing to inflammation and tissue damage. This study investigated ATP
Area of Science:
- Pulmonary Medicine
- Immunology
- Biochemistry
Background:
- Extracellular adenosine triphosphate (ATP) is known to promote inflammation.
- The specific role of extracellular ATP in the pathogenesis of chronic obstructive pulmonary disease (COPD) remains largely unknown.
Purpose of the Study:
- To investigate the expression and functional consequences of extracellular ATP in never-smokers, asymptomatic smokers, and patients with COPD.
- To analyze ATP concentrations and purinergic receptor expression in relation to COPD severity.
Main Methods:
- Quantified ATP in bronchoalveolar lavage fluid (BALF) from never-smokers, asymptomatic smokers, and COPD patients.
- Measured purinergic receptor expression on airway macrophages and blood neutrophils.
- Assessed mediator release and neutrophil chemotaxis following ATP stimulation.
Main Results:
- Elevated BALF ATP concentrations were observed in chronic smokers, with further increases upon acute smoke exposure.
- COPD patients exhibited the highest BALF ATP levels, which correlated negatively with lung function and positively with neutrophil counts.
- ATP stimulation enhanced neutrophil chemotaxis and elastase release, and induced greater pro-inflammatory and tissue-degrading mediator secretion from macrophages in COPD patients, accompanied by up-regulated purinergic receptors.
Conclusions:
- Chronic obstructive pulmonary disease is characterized by significant and sustained upregulation of extracellular ATP in the airways.
- Extracellular ATP plays a crucial role in COPD pathogenesis by exacerbating inflammation and promoting tissue degradation.
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