The Effects of Smoking Cessation on the Risk of Chronic Obstructive Pulmonary Disease Exacerbations

Au, David H.; Bryson, Christopher L.; Chien, Jason W.; Sun, Haili; Udris, Edmunds M.; Evans, Laura; Bradley, Katharine A.

doi:10.1007/s11606-009-0907-y

Cited by 151 publications

(117 citation statements)

References 36 publications

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“…Additionally, enhanced activation of primed NK cells following infection may activate the adaptive immune response. supported by observations that COPD patients who stop smoking have significantly reduced frequency of exacerbations (32,33), which we hypothesize to be due to loss of NK cell priming.…”

Section: Discussionsupporting

confidence: 72%

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Chronic Cigarette Smoke Exposure Primes NK Cell Activation in a Mouse Model of Chronic Obstructive Pulmonary Disease

Motz¹,

Eppert²,

Wortham³

et al. 2010

The Journal of Immunology

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Chronic obstructive pulmonary disease (COPD) is a debilitating, progressive lung disease punctuated by exacerbations of symptoms. COPD exacerbations are most often associated with viral infections, and exposure to cigarette smoke (CS) followed by viral infection has been shown experimentally to enhance lung inflammation, tissue destruction, and airway fibrosis. Despite this, however, the cellular mechanisms responsible for this effect are unknown. In this study, we examined NK cell function in a mouse model of COPD given the vital role of NK cells following viral infection. Ex vivo stimulation of lung leukocytes with poly(I:C), ssRNA40, or ODN1826 enhanced production of NK cell-derived IFN-γ in CS-exposed mice. NK cells from CS-exposed mice exhibited a novel form of priming; highly purified NK cells from CS-exposed mice, relative to NK cells from filtered air-exposed mice, produced more IFN-γ following stimulation with IL-12, IL-18, or both. Further, NK cell priming was lost following smoking cessation. NKG2D stimulation through overexpression of Raet1 on the lung epithelium primed NK cell responsiveness to poly(I:C), ssRNA40, or ODN1826 stimulation, but not cytokine stimulation. In addition, NK cells from CS-exposed mice expressed more cell surface CD107a upon stimulation, demonstrating that the NK cell degranulation response was also primed. Together, these results reveal a novel mechanism of activation of the innate immune system and highlight NK cells as important cellular targets in controlling COPD exacerbations.

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Section: Discussionsupporting

confidence: 72%

“…Several reports indicate that the numbers of COPD exacerbations in patients are reduced following cigarette smoking cessation (32,33). We therefore examined whether NK cell priming persisted after smoking cessation.…”

Section: Nk Cell Priming Is Lost Following Cs Cessationmentioning

confidence: 99%

Chronic Cigarette Smoke Exposure Primes NK Cell Activation in a Mouse Model of Chronic Obstructive Pulmonary Disease

Motz¹,

Eppert²,

Wortham³

et al. 2010

The Journal of Immunology

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“…This result confirms the previous findings of Steuten et al, 15 where the proportion of smokers in a DMP was seen to decrease from 40% to 36% over a 12-month period. Au et al 25 showed within a cohort study of 23,971 current and past smokers that smoking cessation was associated with a reduced risk of exacerbations. Reimbursing the costs of smoking cessation therapy has been shown to be both efficacious 26 and cost-effective.…”

Section: Discussionmentioning

confidence: 99%

Disease Management Programs for Patients With COPD in Germany: A Longitudinal Evaluation of Routinely Collected Patient Records

et al. 2013

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INTRODUCTION:The primary aim of the disease management program (DMP) for patients with COPD is to improve health outcomes and thereby to reduce overall costs. Six years after its introduction in Germany, no consensus has yet been reached as to whether the DMP has been effective in reaching these goals. The objective of the study was an evaluation of the DMP for COPD in Bavaria using routinely collected subject medical records. METHODS: A longitudinal population-based study, comparing the total DMP population of up to 86,560 patients with a stable cohort of 17,549 subjects over a period of 5 years. The effect of subject dropout in the cohort is further estimated by means of inverse probability weighting. RESULTS: The proportion of subjects in the total population who were prescribed and received treatment with oral corticosteroids declined at a constant rate of 1.0% per year (P < .001). The proportion of subjects who were given a prescription for theophylline decreased at a constant rate of 2.0% per year (P < .001). By 2012, 15.6% of the total population and 26% of the cohort had undergone self-management education. While the proportion of smokers in the total population remained constant because of the effect of newly enrolled subjects, the proportion of smokers decreased significantly even after dropout adjustment, from 29% to 21%. The occurrence of exacerbations decreased steadily at a rate of 0.9% (total population) or 0.7% (cohort) per year. While the occurrence of emergency hospital admissions decreased in the total population, an increase was observed within the cohort. CONCLUSIONS: Summarizing all results leads to the suggestion that the German DMP for COPD has been effective in enhancing the quality of care in regard to an improved adherence to guidelines, pharmacotherapy, exacerbations, and self-management education. However, the DMP was not able to prevent an increase in emergency hospital admissions for the stable population in the cohort.

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“…Several large observational studies with long follow-up suggest that smoking cessation decreases the risk (relative to continued smoking) of incident COPD and hospital admission with a COPD exacerbation [9]. The risk reduction of COPD exacerbations varies with duration of time since quitting smoking and cumulative tobacco exposure (pack-years of smoking) [20]. According to a study conducted in Denmark, self-reported smoking cessation was associated with a reduction in the risk of COPD morbidity of approximately 40% [21].…”

Section: Discussionmentioning

confidence: 99%

COPD Morbidity and Mortality in Ukraine after Tobacco Control Policies Implementation

Andreeva¹,

Krasovsky²

2017

Chron Obstruct Pulmon Dis

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Tobacco is a known cause of COPD and smoking cessation is known reduce the risk of developing COPD. Whether tobacco control policies resulting in decreased prevalence of smoking are followed by short-term changes of morbidity and mortality indicators is unknown. We explored how recent successes in tobacco control in Ukraine are reflected in routinely collected data related to COPD. Methods:We used publicly available sources of information:European Mortality database for standardized death rates and aggregated results from panel household surveys with questions on any and respiratory chronic diseases for morbidity. Results:In early 1980s, chronic pulmonary mortality in Ukraine was 25-30 deaths/100 000, it increased to almost 60/100 000 in 1995 and then was steadily declining to 18/100 000 in 2010s. The upward mortality trend in 1987-95 was more expressed in middle-aged people compared with older ones. The declining mortality trend after 1995 was accelerating over time, was similar among men and women and much faster in middle-aged people than in older ones. The accelerated decline of respiratory mortality was observed during the economic recession of late 1990-s and in years of increased cigarette real prices. The dynamics of self-reported major chronic noncommunicable diseases reveals the decline in chronic bronchitis and emphysema from 33/1000 in 2008 to 23/1000 in 2012, while no changes were observed in all chronic, cardiovascular diseases and cancer. Conclusion:Major changes in COPD mortality in 1980-2010 were concurrent with changing economic conditions and could only partially be tobacco-related. Tobacco control policies, conducted in Ukraine since 2005 could accelerate then happening COPD mortality decline. In the time of both mortality increase and decrease, middle-aged people reacted faster than those older ones, probably due to greater role of behavioral factors in younger people. COPD morbidity started to decrease only since 2009 when cigarettes became much less affordable.

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The Effects of Smoking Cessation on the Risk of Chronic Obstructive Pulmonary Disease Exacerbations

Cited by 151 publications

References 36 publications

Chronic Cigarette Smoke Exposure Primes NK Cell Activation in a Mouse Model of Chronic Obstructive Pulmonary Disease

Chronic Cigarette Smoke Exposure Primes NK Cell Activation in a Mouse Model of Chronic Obstructive Pulmonary Disease

Disease Management Programs for Patients With COPD in Germany: A Longitudinal Evaluation of Routinely Collected Patient Records

COPD Morbidity and Mortality in Ukraine after Tobacco Control Policies Implementation

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