Influence of smoking on airway inflammation and remodelling in asthma

St-Laurent, Julie; Bergeron, C.; Pagé, Nathalie; Couture, Christian; Laviolette, Michel; Lp, Boulet

doi:10.1111/j.1365-2222.2008.03032.x

Cited by 69 publications

(39 citation statements)

References 45 publications

(59 reference statements)

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“…152 In a small but interesting study analyzing bronchial biopsy specimens from steroid-naive young patients with mild asthma, the bronchial mucosa from smoking asthmatic patients showed squamous cell metaplasia and increased expression of neutrophil elastase, IFN-g, and IL-8, which might contribute to an impaired response to therapy and poor clinical outcome. 153 …”

Section: Viral Infection and Remodelingmentioning

confidence: 97%

Remodeling in asthma

Al‐Muhsen¹,

Johnson²,

Hamid³

2011

Journal of Allergy and Clinical Immunology

365

293

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Section: Viral Infection and Remodelingmentioning

confidence: 97%

Remodeling in asthma

Al‐Muhsen¹,

Johnson²,

Hamid³

2011

Journal of Allergy and Clinical Immunology

365

293

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“…Induced sputum in both healthy smokers [10] and in steroid-naive asthmatic smokers [23] contains higher numbers of neutrophils than in their nonsmoking counterparts. Increased expression of intraepithelial IL8, a potent neutrophil chemoattractant, has been detected in bronchial biopsies of smoking asthmatics compared to asthmatic nonsmokers [25], and its release is augmented by exposure to cigarette smoke [26]. IL8 correlates positively with the number of neutrophils in sputum, and increases significantly with increasing pack-years [23].…”

Section: Discussionmentioning

confidence: 99%

Smoking Attenuates Increase in Exhaled Nitric Oxide in Atopic but Not in Nonatopic Young Adults with Asthma

Rouhos

Ekroos²,

Karjalainen

et al. 2010

Int Arch Allergy Immunol

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Background: Measurement of fractional exhaled nitric oxide (FENO) is useful in assessing eosinophilic airway inflammation. Smoking may modify airway inflammation and reduce FENO levels, compromising the diagnostic value of FENO in smokers. How smoking influences FENO in atopic versus nonatopic asthmatics is unknown. The aim of the present study was to compare FENO in atopic and nonatopic steroid-naive young asthmatic adults and in healthy subjects in terms of smoking. Methods: Forty-six (30 atopic) smoking and 70 (54 atopic) nonsmoking steroid-naive army conscripts (mean age 20 years) with current symptomatic asthma underwent FENO measurement, skin prick tests, spirometry with a bronchodilation test, bronchial histamine challenge, and a standardized exercise test. Ten healthy smokers and 9 healthy nonsmokers underwent FENO measurement, spirometry and bronchial histamine challenge. Results: Smokers with asthma showed significantly higher FENO than did healthy smokers and nonsmokers (p = 0.001, both comparisons). Among atopic asthmatics, FENO was lower in smokers than in nonsmokers (p = 0.002) whereas among nonatopic asthmatics no such difference was detectable (p = 0.89). However, even among nonatopic asthmatic smokers FENO was significantly higher than among healthy controls (p = 0.01). Conclusion: Smoking seems to attenuate the increase in FENO in atopic but not in nonatopic asthmatics. This finding suggests differences in biochemical mechanisms of NO formation in atopic and nonatopic asthma. However, FENO was significantly higher both in atopic and nonatopic asthmatic smokers than in healthy controls. This suggests that FENO can be applied for diagnostic purposes also in young adult smokers.

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“…LANGE et al [106] also have demonstrated an accelerated decline in pulmonary function in people with asthma, which is even more marked in those who smoke. Furthermore, smoking is associated with neutrophilic airway inflammation, more difficult-to-control asthma and a reduced response to inhaled corticosteroids [105,107,[113][114][115].…”

Section: Copd and Smokingmentioning

confidence: 99%

Influence of comorbid conditions on asthma

Lp¹

2009

European Respiratory Journal

Self Cite

215

169

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Various conditions such as rhinosinusitis, gastro-oesophageal reflux disease, psychological disturbances, chronic infections and obstructive sleep apnoea are often observed in asthmatic patients and may affect asthma control and outcomes. These comorbidities may change the asthma phenotype, be part of the same pathophysiological process, act as confounding factors in the diagnosis or assessment of control of asthma, and/or result from specific environmental exposures. The influences of these conditions on asthma are variable and for many of them still uncertain; nevertheless, they may alter asthma responses to current therapy. A systematic evaluation and an appropriate treatment of asthma-associated comorbid conditions should be part of asthma management, particularly for severe disease. With regard to clinical research, associated conditions may influence the results of trials and should be taken into account in the subjects' inclusion criteria and analysis of data.

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Influence of smoking on airway inflammation and remodelling in asthma

Abstract: Smoking status modifies morphological and inflammatory processes in young subjects with mild asthma. The changes may possibly affect asthma treatment responses and clinical outcomes.

Cited by 69 publications

References 45 publications

Remodeling in asthma

Remodeling in asthma

Smoking Attenuates Increase in Exhaled Nitric Oxide in Atopic but Not in Nonatopic Young Adults with Asthma

Influence of comorbid conditions on asthma

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