COPD: the dangerous underestimate of 15%

Rennard, Stephen I.; Vestbo, Jørgen

doi:10.1016/s0140-6736(06)68516-4

Cited by 233 publications

(172 citation statements)

References 14 publications

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“…The economic burden of COPD is measured by the billions of dollars in the United States, and increasing worldwide prevalence will place additional strains on the global economy (1). The chief cause of COPD is long term cigarette smoking, and most smokers will develop COPD if smokingrelated, extrapulmonary diseases do not claim their lives beforehand (2). In conjunction with smoking, the development of COPD is modified by genetics, environmental exposures (e.g., air pollution and occupational exposures), and infections (3,4).…”

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confidence: 99%

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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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confidence: 99%

“…These pulmonary maladies result from inflammation, mucus hypersecretion, and alveolar destruction (4). The inflammation is a strong correlate of disease severity in patients and is critically involved in disease development experimentally (2,4,5). Attention has traditionally been centered on the roles of macrophages and neutrophils in disease development (4).…”

mentioning

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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“…However, fewer than 50% of smokers develop COPD [9]. The socioeconomic status may be linked to a child's birth weight.…”

Section: Factors Influencing Disease Development and Progressionmentioning

confidence: 99%

The View of the Turkish Thoracic Society on the Report of the GOLD 2017 Global Strategy for the Diagnosis, Management, and Prevention of COPD

Köktürk¹,

Gürgün²,

Şen³

et al. 2017

Turk Thorac J

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Since the Global Initiative for Obstructive Lung Disease (GOLD) published its first guidelines on chronic obstructive pulmonary disease (COPD) in 2001, much has changed till 2017. Previous versions of GOLD guidelines mentioned the forced expiratory volume in one second (FEV 1 )-based approach for staging and treatment modalities. Since 2011, a composite multi-dimensional approach has been introduced to cover various aspects of the disease. Unfortunately, this approach was not found to be correlated with mortality as well as the FEV 1 -based approach, despite the fact that it was better for estimating exacerbation rates. Although this assessment tool has been considered as a big step in personalized medicine, the system was rather complex to use in daily practice. In 2017, GOLD introduced a major revision in many aspects of the disease. This mainly includes a revised assessment tool and treatment algorithm. This new ABCD algorithm has excluded spirometry for guiding pharmacological therapy. Treatment recommendations are mainly based on symptoms and exacerbation rates. Escalation and de-escalation strategies have been proposed for the first time. The spirometric measurement has only been retained to confirm the diagnosis and lead to nonpharmacological therapies. In this report, the Turkish Thoracic Society COPD assembly aimed to summarize and give an insight to the Turkish interpretation of GOLD 2017.

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“…This has been rounded off and incorrectly quoted as: "15% of smokers will get COPD." In fact, while susceptibility is variable, more than 50% of smokers will develop the airflow limitation criteria for COPD 54,55 , though the majority remain undiagnosed 56 . The majority of the undiagnosed COPD patients generally have milder airflow limitation, which has raised the question of what is clinically important COPD.…”

Section: Clinically Important Chronic Obstructive Pulmonary Diseasementioning

confidence: 99%

The Natural History of COPD: Beyond Fletcher and Peto

Rennard¹,

Agustí²,

Vestbo³

2015

BRN

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The landmark publication of the "British Postal Worker Study" by Fletcher and colleagues in the 1970s established that chronic obstructive pulmonary disease occurs because smoking exposure in susceptible individuals accelerates the decline of lung function that occurs physiologically with age. In the 40 years since Fletcher et al. published the results of their study, subsequent research has advanced our understanding of chronic obstructive pulmonary disease and its natural history. The current review focuses on areas where the proposal by Fletcher et al. require expansion and/or modification, including: (i) the recognition of the role of exposures other than cigarette smoking (or even in its absence where chronic obstructive pulmonary disease may be related to other conditions such as asthma); (ii) that smoking affects a larger percentage of individuals than suggested by Fletcher et al.; (iii) that the benefits of smoking cessation vary with age/disease severity; (iv) that lung function decline does not accelerate with advancing age; (v) that many can develop chronic obstructive pulmonary disease with "normal" rates of lung function decline if they have abnormal lung growth and, therefore, low lung function at early age; (vi) that the relationship between mucus hypersecretion, exacerbations, and lung function decline is more complex than suggested by Fletcher et al.; and, finally, (vii) Corresponding author: Stephen I. Rennard, srennard@unmc.edu

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COPD: the dangerous underestimate of 15%

Cited by 233 publications

References 14 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

The View of the Turkish Thoracic Society on the Report of the GOLD 2017 Global Strategy for the Diagnosis, Management, and Prevention of COPD

The Natural History of COPD: Beyond Fletcher and Peto

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