Effects of Smoking Cessation on Lung Function and Airway Inflammation in Smokers with Asthma

Chaudhuri, Rekha; Livingston, Eric W.; McMahon, Alex D.; Lafferty, Jane; Fraser, Iona; Spears, Mark; McSharry, Charles; Thomson, Neil C.

doi:10.1164/rccm.200510-1589oc

Cited by 281 publications

(235 citation statements)

References 48 publications

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“…Obesity is associated with both childhood and adult onset severe asthma, but the impact of obesity may differ by age at onset and degree of allergic inflammation [27,28]. Tobacco smoke and environmental air pollution are routinely linked as risk factors for more severe asthma [29,30]. Both personal smoking and obesity have been linked to corticosteroid insensitivity, also associated with severe asthma [31,32].…”

Section: Geneticsmentioning

confidence: 99%

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International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma

et al. 2013

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Severe or therapy-resistant asthma is increasingly recognised as a major unmet need. A Task Force, supported by the European Respiratory Society and American Thoracic Society, reviewed the definition and provided recommendations and guidelines on the evaluation and treatment of severe asthma in children and adults.A literature review was performed, followed by discussion by an expert committee according to the GRADE (Grading of Recommendations, Assessment, Development and Evaluation) approach for development of specific clinical recommendations.When the diagnosis of asthma is confirmed and comorbidities addressed, severe asthma is defined as asthma that requires treatment with high dose inhaled corticosteroids plus a second controller and/or systemic corticosteroids to prevent it from becoming “uncontrolled” or that remains “uncontrolled” despite this therapy. Severe asthma is a heterogeneous condition consisting of phenotypes such as eosinophilic asthma. Specific recommendations on the use of sputum eosinophil count and exhaled nitric oxide to guide therapy, as well as treatment with anti-IgE antibody, methotrexate, macrolide antibiotics, antifungal agents and bronchial thermoplasty are provided.Coordinated research efforts for improved phenotyping will provide safe and effective biomarker-driven approaches to severe asthma therapy.

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Section: Geneticsmentioning

confidence: 99%

“…Smoking appears to alter the inflammatory process which may contribute to their reported lower responses to corticosteroid therapy [29,32]. Environmental tobacco smoke exposure is also associated with adverse asthma outcomes in children and adults [30].…”

Section: Remarksmentioning

confidence: 99%

International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma

et al. 2013

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“…A long‐lasting effect after smoking cessation in asthmatics on corticosteroid responsiveness has also been suggested by the observation of an attenuated response to corticosteroid treatment in former smokers with asthma (Chaudhuri et al. 2006). To investigate whether DNA methylation was involved in the observed effects of CS exposure on periostin expression, we used the demethylating agent 5‐aza during CS exposure.…”

Section: Discussionmentioning

confidence: 99%

Cigarette smoke differentially affects IL-13-induced gene expression in human airway epithelial cells

et al. 2017

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Allergic airways inflammation in asthma is characterized by an airway epithelial gene signature composed of POSTN,CLCA1, and SERPINB2. This Th2 gene signature is proposed as a tool to classify patients with asthma into Th2‐high and Th2‐low phenotypes. However, many asthmatics smoke and the effects of cigarette smoke exposure on the epithelial Th2 gene signature are largely unknown. Therefore, we investigated the combined effect of IL‐13 and whole cigarette smoke (CS) on the Th2 gene signature and the mucin‐related genes MUC5AC and SPDEF in air–liquid interface differentiated human bronchial (ALI‐PBEC) and tracheal epithelial cells (ALI‐PTEC). Cultures were exposed to IL‐13 for 14 days followed by 5 days of IL‐13 with CS exposure. Alternatively, cultures were exposed once daily to CS for 14 days, followed by 5 days CS with IL‐13. POSTN,SERPINB2, and CLCA1 expression were measured 24 h after the last exposure to CS and IL‐13. In both models POSTN,SERPINB2, and CLCA1 expression were increased by IL‐13. CS markedly affected the IL‐13‐induced Th2 gene signature as indicated by a reduced POSTN,CLCA1, and MUC5AC expression in both models. In contrast, IL‐13‐induced SERPINB2 expression remained unaffected by CS, whereas SPDEF expression was additively increased. Importantly, cessation of CS exposure failed to restore IL‐13‐induced POSTN and CLCA1 expression. We show for the first time that CS differentially affects the IL‐13‐induced gene signature for Th2‐high asthma. These findings provide novel insights into the interaction between Th2 inflammation and cigarette smoke that is important for asthma pathogenesis and biomarker‐guided therapy in asthma.

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“…To the best of the current authors' knowledge, this is the first study to report on this matter, as most previous studies addressing atopy versus smoking have focused on the tobacco-induced increased risk of developing atopy and asthma [21,22] and on the increased severity, inflammation and progress of atopic diseases, such as asthma in smokers [23][24][25].…”

Section: Discussionmentioning

confidence: 99%

Impact of acute exposure to tobacco smoke on gelatinases in the bronchoalveolar space

Glader

Eldh²,

Bozinovski³

et al. 2008

Eur Respir J

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Clinical studies have indicated increased gelatinase activity in the airways of patients suffering from chronic obstructive pulmonary disease caused by tobacco smoke. The present study aimed to determine whether acute exposure to tobacco smoke per se causes a substantial and lasting impact on gelatinases and their inhibitors in the peripheral airways of atopic and nonatopic human subjects.Bronchoscopy with bronchoalveolar lavage (BAL) was performed on occasional smokers with and without atopy before and after smoking 10 cigarettes over a 48-h period. Samples from a group of never-smokers not exposed to tobacco smoke served as controls. Gelatinase identity and activity were measured using zymography, and gelatinase activity assay and concentrations of matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of MMP (TIMP)-1 and TIMP-2 were measured using ELISA.The results revealed no pronounced changes in identity, net activity or concentration of the gelatinases or changes in concentrations of TIMP-1 and TIMP-2 in BAL fluid before and after acute exposure to tobacco smoke.In conclusion, the present experimental study indicates that acute exposure to tobacco smoke does not cause any substantial impact on gelatinases or their inhibitors in the peripheral airways, irrespective of atopy status, a finding that is compatible with the fact that it takes many years of tobacco smoking to establish chronic obstructive pulmonary disease. KEYWORDS: Chronic obstructive pulmonary disease, macrophage, matrix metalloproteinase 9, neutrophils, tissue inhibitor of matrix metalloproteinase

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Effects of Smoking Cessation on Lung Function and Airway Inflammation in Smokers with Asthma

Abstract: By 6 wk after smoking cessation, subjects who quit smoking had achieved considerable improvement in lung function and a fall in sputum neutrophil count compared with subjects who continued to smoke. These findings highlight the importance of smoking cessation in asthma.

Cited by 281 publications

References 48 publications

International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma

International ERS/ATS guidelines on definition, evaluation and treatment of severe asthma

Cigarette smoke differentially affects IL-13-induced gene expression in human airway epithelial cells

Impact of acute exposure to tobacco smoke on gelatinases in the bronchoalveolar space

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