Reversibility of Airways Injury over a 12-Month Period following Smoking Cessation

Swan, Gary E.; Hodgkin, John E.; Roby, Tina J.; Mittman, Charles; Jacobo, Nancy; Peters, James M.

doi:10.1378/chest.101.3.607

Cited by 30 publications

(19 citation statements)

References 6 publications

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“…The number of macrophages, the percentage of eosinophils and IL-8 levels in sputum decreased significantly after 12 months smoking cessation, which is in agreement with the results of previous studies in BAL fluid and sputum [10][11][12]14]. In addition, previous results have shown that in long-term exsmokers, macrophages in bronchial biopsies are lower than in ex-smokers with COPD [9].…”

Section: Discussionsupporting

confidence: 91%

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Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers

Willemse

Hacken

Rutgers

et al. 2006

Respiratory Medicine: COPD Update

120

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Smoking cessation is the only treatment in patients with chronic obstructive pulmonary disease (COPD) effective in slowing down disease progression. Its effect on airway inflammation in COPD is unknown, although cross-sectional studies suggest ongoing inflammation in ex-smokers.In order to elucidate the effect of smoking cessation on airway inflammation, 28 smokers with COPD (mean age: 55 yrs; forced expiratory volume in one second: 71% predicted) and 25 asymptomatic smokers with normal lung function (aged 50 yrs) were included in a 1-yr smoking cessation programme. Effects of smoking cessation on airway inflammation were investigated in bronchial biopsies (baseline, 12 months) and sputum samples (baseline, 2, 6 and 12 months).In the 12 candidates with COPD who successfully ceased smoking, airway inflammation persisted in bronchial biopsies, while the number of sputum neutrophils, lymphocytes, interleukin (IL)-8 and eosinophilic-cationic-protein levels significantly increased at 12 months. In the 16 asymptomatic smokers who successfully quitted, inflammation significantly reduced (i.e. number of sputum macrophages, percentage of eosinophils and IL-8 levels) or did not change.The current authors suggest that the observed persistent airway inflammation in patients with chronic obstructive pulmonary disease is related to repair of tissue damage in the airways. It remains to be elucidated whether this reflects a beneficial or detrimental effect.

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Section: Discussionsupporting

confidence: 91%

“…the number of macrophages and neutrophils [10][11][12][13][14][15][16]. This suggests that the inflammatory changes in the airways due to smoking are reversible in smokers without COPD.…”

mentioning

confidence: 99%

Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers

Willemse

Hacken

Rutgers

et al. 2006

Respiratory Medicine: COPD Update

120

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“…The autofluorescence characteristic of smokers' macrophages, which presumably reflects engulfed particles, remained elevated for 15 months. A similar change in inflammatory cells following smoking cessation was observed in sputum of normal smokers by SWAN et al [23].…”

Section: Smoking Cessation and Pulmonary Inflammationsupporting

confidence: 80%

Inflammation in COPD: a link to systemic comorbidities

Rennard¹

2007

Eur Respir Rev

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Chronic obstructive pulmonary disease (COPD) has been defined as a preventable and treatable disease characterised by progressive airflow limitation that is not fully reversible and associated with an abnormal inflammatory response in the lungs.Results from a large number of recent studies have characterised the inflammatory processes underlying COPD. Inflammatory cells, most notably CD8+ T-lymphocytes, macrophages and neutrophils, as well as a large number of chemokines, cytokines and proteinases, are believed to play a role.The inflammatory processes in COPD contribute to remodelling of pulmonary tissues, leading to the irreversible airflow limitation characteristic of this disease. Inflammation may also contribute to the comorbidities often observed in COPD patients. Patients with COPD often have cardiovascular disease, changes in body composition, osteoporosis and anaemia. The same inflammatory processes that characterise COPD are also risk factors for these comorbidities.Ongoing studies are evaluating a wide range of new therapies for chronic obstructive pulmonary disease. Some of these have the potential to blunt the inflammatory processes underlying chronic obstructive pulmonary disease and potentially the associated comorbid conditions. These therapies may significantly improve survival, function and quality of life for patients with this disease.

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“…Smoking cessation has also been shown to decrease airway injury and lower levels of mucus in exfoliated sputum tracheobronchial cells compared with those who continued to smoke (71). A large longitudinal follow-up study found that the incidence rates of CB were much higher in current smokers compared with ex-smokers (42 vs. 26%) (22).…”

Section: Smoking Cessationmentioning

confidence: 99%

Chronic Bronchitis and Chronic Obstructive Pulmonary Disease

Kim

Criner

2013

Am J Respir Crit Care Med

388

276

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Chronic bronchitis (CB) is a common but variable phenomenon in chronic obstructive pulmonary disease (COPD). It has numerous clinical consequences, including an accelerated decline in lung function, greater risk of the development of airflow obstruction in smokers, a predisposition to lower respiratory tract infection, higher exacerbation frequency, and worse overall mortality. CB is caused by overproduction and hypersecretion of mucus by goblet cells, which leads to worsening airflow obstruction by luminal obstruction of small airways, epithelial remodeling, and alteration of airway surface tension predisposing to collapse. Despite its clinical sequelae, little is known about the pathophysiology of CB and goblet cell hyperplasia in COPD, and treatment options are limited. In addition, it is becoming increasingly apparent that in the classic COPD spectrum, with emphysema on one end and CB on the other, most patients lie somewhere in the middle. It is known now that many patients with severe emphysema can develop CB, and small airway pathology has been linked to worse clinical outcomes, such as increased mortality and lesser improvement in lung function after lung volume reduction surgery. However, in recent years, a greater understanding of the importance of CB as a phenotype to identify patients with a beneficial response to therapy has been described. Herein we review the epidemiology of CB, the evidence behind its clinical consequences, the current understanding of the pathophysiology of goblet cell hyperplasia in COPD, and current therapies for CB.Keywords: chronic obstructive pulmonary disease; chronic bronchitis; goblet cell hyperplasia; N-acetylcysteine; roflumilast Chronic obstructive pulmonary disease (COPD) is a common disease characterized by irreversible airflow obstruction and persistent inflammation to noxious environmental stimuli, usually cigarette smoke. It affects 12 to 16 million people in the United States and is the third leading cause of death and disease burden worldwide (1). COPD encompasses a spectrum of diseases, with chronic bronchitis (CB) at one end and emphysema at the other, with most individuals having some characteristics of both. The CB definition used in epidemiologic studies has been variable, but the classic definition is chronic cough and sputum production for at least 3 months per year for two consecutive years (2). CB has numerous clinical consequences, including an increased exacerbation rate, accelerated decline in lung function, worse health-related quality of life (HRQoL), and possibly increased mortality (3-6). We review the clinical phenotype of CB, the current understanding of its pathophysiology, and treatment options. EPIDEMIOLOGYCB is common in the general population. Table 1 provides an overview of the prevalence of cough and sputum production in population-based studies. CB is seen in 3.4 to 22.0% of adults (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19). This wide range of prevalence estimates may be due to varying definitions of CB (i.e., chronic phlegm ver...

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Reversibility of Airways Injury over a 12-Month Period following Smoking Cessation

Cited by 30 publications

References 6 publications

Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers

Effect of 1-year smoking cessation on airway inflammation in COPD and asymptomatic smokers

Inflammation in COPD: a link to systemic comorbidities

Chronic Bronchitis and Chronic Obstructive Pulmonary Disease

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