Association of current smoking with airway inflammation in chronic obstructive pulmonary disease and asymptomatic smokers

Willemse, Brigitte; Hacken, Nick H. T. ten; Rutgers, Bea; Postma, Dirkje S.; Timens, Wim

doi:10.1016/j.rmedu.2005.09.009

Cited by 10 publications

(15 citation statements)

References 33 publications

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“…Bronchial biopsy and sputum material of 11 COPD and 15 asymptomatic smoking subjects who successfully stopped smoking for at least 1 year from the study of Willemse et al were studied (patient characteristics; Table 1) [5,4,15]. In short, the main important inclusion and exclusion criteria for both groups were: COPD (according to the American Thoracic Society (ATS)/ European Respiratory Society (ERS) guidelines [16]): forced expiratory volume (FEV) 1 / forced vital capacity post-bronchodilator <0.7, and chronic respiratory symptoms for at least 3 months for two successive years.…”

Section: Subjectsmentioning

confidence: 99%

Adenosine receptors in COPD and asymptomatic smokers: effects of smoking cessation

et al. 2009

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Our group has shown that 1-year smoking cessation persisted or increased airway inflammation in chronic obstructive pulmonary disease (COPD). We compared adenosine and adenosine receptor (AR) expression in COPD and asymptomatic smokers (AS) before and after 1-year smoking cessation. Sputum cytospins and bronchial biopsies of (ex)smoking COPD patients and AS were studied for A(1)R, A(2A)R, A(2B)R, and A(3)R expression. Adenosine and inflammatory mediators were measured in sputum supernatants. At baseline, COPD patients had lower levels of adenosine and higher levels of vascular endothelial growth factor in sputum than AS. Smoking cessation induced significantly different effects in COPD than in AS, i.e. an increase in percentages of A(3)R expressing neutrophils and A(1)R expressing macrophages in COPD as increase in adenosine and monocyte chemoattractant protein-1 levels in sputum. Adenosine-related effector mechanisms may contribute to the persistence and progression of airway inflammation in COPD following 1-year smoking cessation.

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Section: Subjectsmentioning

confidence: 99%

Adenosine receptors in COPD and asymptomatic smokers: effects of smoking cessation

et al. 2009

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“…There are currently no specific COPD treatments, and smoking cessation remains the most effective therapeutic intervention (Scanlon et al, ). Several studies in humans and animals demonstrated that, once COPD is initiated, the pulmonary inflammatory response continues (De Cunto et al, ; Gamble et al, ; Lapperre et al, ; Scanlon et al, ; Willemse, ten Hacken, Rutgers, Postma, & Timens, ), leading to a progressive loss of alveolar wall that cannot be reversed. Abnormal amounts of sphingomyelinase have been found in smokers with emphysema and the increased ceramide levels in alveolar septal cells and macrophages well correlated to lung destruction and dysfunction (Petrache et al, ; Petrache et al, ; Telenga et al, ).…”

Section: Introductionmentioning

confidence: 99%

Functional contribution of sphingosine‐1‐phosphate to airway pathology in cigarette smoke‐exposed mice

Cunto

Brancaleone

Riemma

et al. 2019

British J Pharmacology

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Background and Purpose: A critical role for sphingosine kinase/sphingosine-1phosphate (S1P) pathway in the control of airway function has been demonstrated in respiratory diseases. Here, we address S1P contribution in a mouse model of mild chronic obstructive pulmonary disease (COPD).Experimental Approach: C57BL/6J mice have been exposed to room air or cigarette smoke up to 11 months and killed at different time points. Functional and molecular studies have been performed.Key Results: Cigarette smoke caused emphysematous changes throughout the lung parenchyma coupled to a progressive collagen deposition in both peribronchiolar and peribronchial areas. The high and low airways showed an increased reactivity to cholinergic stimulation and α-smooth muscle actin overexpression. Similarly, an increase in airway reactivity and lung resistances following S1P challenge occurred in smoking mice. A high expression of S1P, Sph-K 2 , and S1P receptors (S1P 2 and S1P 3 ) has been detected in the lung of smoking mice. Sphingosine kinases inhibition reversed the increased cholinergic response in airways of smoking mice.Conclusions and Implications: S1P signalling up-regulation follows the disease progression in smoking mice and is involved in the development of airway hyperresponsiveness. Our study defines a therapeutic potential for S1P inhibitors in management of airways hyperresponsiveness associated to emphysema in smokers with both asthma and COPD.

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“…Several research groups have demonstrated increased adherence of bacteria to respiratory epithelial cells of smokers, compared with nonsmokers [16][17][18][19]. Finally, tobacco smoke induces inflammation, which may result in epithelial injury, predisposing to bacterial colonization [20].…”

mentioning

confidence: 99%

Otitis Media, Bacterial Colonization, and the Smoking Parent

Murphy¹

2006

Clinical Infectious Diseases

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Association of current smoking with airway inflammation in chronic obstructive pulmonary disease and asymptomatic smokers

Cited by 10 publications

References 33 publications

Adenosine receptors in COPD and asymptomatic smokers: effects of smoking cessation

Adenosine receptors in COPD and asymptomatic smokers: effects of smoking cessation

Functional contribution of sphingosine‐1‐phosphate to airway pathology in cigarette smoke‐exposed mice

Otitis Media, Bacterial Colonization, and the Smoking Parent

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