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Critical role of aldehydes in cigarette smoke-induced acute airway inflammation

This paper is available in a repository.
This paper is available in a repository.

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Abstract

Background: Cigarette smoking (CS) is the most important risk factor for COPD, which is associated with neutrophilic airway inflammation. We hypothesize, that highly reactive aldehydes are critical for CS-induced neutrophilic airway inflammation. Methods: BALB/c mice were exposed to CS, water filtered CS (WF-CS) or air for 5 days. Levels of total particulate matter (TPM) and aldehydes in CS and WF-CS were measured. Six hours after the last exposure, inflammatory cells and cytokine levels were measured in lung tissue and bronchoalveolar lavage fluid (BALF). Furthermore, Beas-2b bronchial epithelial cells were exposed to CS extract (CSE) or WF-CS extract (WF-CSE) in the absence or presence of the aldehyde acrolein and IL-8 production was measured after 24 hrs. Results: Compared to CS, in WF-CS strongly decreased (CS; 271.1 +/- 41.5 mu M, WF-CS; 58.5 +/- 8.2 mu M) levels of aldehydes were present whereas levels of TPM were only slightly reduced (CS; 20.78 +/- 0.59 mg, WF-CS; 16.38 +/- 0.36 mg). The numbers of mononuclear cells in BALF (p Conclusion: Aldehydes present in CS play a critical role in inflammatory cytokine production and neutrophilic- but not mononuclear airway inflammation.