Progression from Asthma to Chronic Obstructive Pulmonary Disease. Is Air Pollution a Risk Factor?

To, Teresa; Zhu, Jingqin; Larsen, Kristian; Simatovic, Jacqueline; Feldman, Laura; Ryckman, Kandace; Gershon, Andrea S.; Lougheed, M. Diane; Licskai, Christopher; Chen, Hong; Villeneuve, Paul J.; Crighton, Eric; Su, Yushan; Sadatsafavi, Mohsen; Williams, Devon; Carlsten, Christopher

doi:10.1164/rccm.201510-1932oc

Cited by 120 publications

(80 citation statements)

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“…Os poluentes atmosféricos têm sido associados, há décadas, à mortalidade e ao agravamento de doenças respirató-rias XIONG et al, 2015;FREITAS et al, 2016;TO et al, 2016) e cardiovasculares (POPE et al, 2004;CHANG et al, 2015;BRAVO et al, 2016;ZÚÑIGA et al, 2016). Dentre as doenças pulmonares, já foi relatado que a poluição do ar agrava o risco de pessoas com asma evoluírem para o quadro de Doença Pulmonar Obstrutiva Crônica (DPOC) em até três vezes mais .…”

Section: Introductionunclassified

Avaliação de impacto à saúde do Programa de Controle de Poluição do Ar por Veículos Automotores no município de São Paulo, Brasil

Abe

Miraglia

2018

Rev. Bras. Ciênc. Ambient. (Online)

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Section: Introductionunclassified

Avaliação de impacto à saúde do Programa de Controle de Poluição do Ar por Veículos Automotores no município de São Paulo, Brasil

Abe

Miraglia

2018

Rev. Bras. Ciênc. Ambient. (Online)

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“…Large-scale attempts to identify biomarkers reflecting COPD subtypes have yielded modest results [17, 18], in which cytokines and air pollution may provide some value as predictive markers for progression [19, 20], albeit new biomarkers are needed [3]. …”

Section: Introductionmentioning

confidence: 99%

Biomarkers of extracellular matrix turnover are associated with emphysema and eosinophilic-bronchitis in COPD

et al. 2017

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BackgroundChronic obstructive pulmonary disease (COPD) is characterized by airflow obstruction and loss of lung tissue mainly consisting of extracellular matrix (ECM). Three of the main ECM components are type I collagen, the main constituent in the interstitial matrix, type VI collagen, and elastin, the signature protein of the lungs. During pathological remodeling driven by inflammatory cells and proteases, fragments of these proteins are released into the bloodstream, where they may serve as biomarkers for disease phenotypes. The aim of this study was to investigate the lung ECM remodeling in healthy controls and COPD patients in the COPDGene study.MethodsThe COPDGene study recruited 10,300 COPD patients in 21 centers. A subset of 89 patients from one site (National Jewish Health), including 52 COPD patients, 12 never-smoker controls and 25 smokers without COPD controls, were studied for serum ECM biomarkers reflecting inflammation-driven type I and VI collagen breakdown (C1M and C6M, respectively), type VI collagen formation (Pro-C6), as well as elastin breakdown mediated by neutrophil elastase (EL-NE). Correlation of biomarkers with lung function, the SF-36 quality of life questionnaire, and other clinical characteristics was also performed.ResultsThe circulating concentrations of biomarkers C6M, Pro-C6, and EL-NE were significantly elevated in COPD patients compared to never-smoking control patients (all p < 0.05). EL-NE was significantly elevated in emphysema patients compared to smoking controls (p < 0.05) and never-smoking controls (p < 0.005), by more than 250%. C1M was inversely associated with forced expiratory volume in 1 s (FEV1) (r = −0.344, p = 0.001), as was EL-NE (r = −0.302, p = 0.004) and Pro-C6 (r = −0.259, p = 0.015). In the patients with COPD, Pro-C6 was correlated with percent predicted Forced Vital Capacity (FVC) (r = 0.281, p = 0.046) and quality of life using SF-36. C6M and Pro-C6, were positively correlated with blood eosinophil numbers in COPD patients (r = 0.382, p = 0.006 and r = 0.351, p = 0.012, respectively).ConclusionsThese data suggest that type VI collagen turnover and elastin degradation by neutrophil elastase are associated with COPD-induced inflammation (eosinophil-bronchitis) and emphysema. Serological assessment of type VI collagen and elastin turnover may assist in identification of phenotypes likely to be associated with progression and amenable to precision medicine for clinical trials.

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“…The global prevalence of COPD, as determined by the World Health Organization, is 11.7% [1], and it is predicted that by 2030 it will be the fourth leading cause of death worldwide [2]. Mainstream or second-hand cigarette smoke exposure is a risk factor for developing COPD [3], which can be exacerbated by genetic factors [4, 5] and environmental exposures [6, 7]. Chronic cigarette smokers that develop COPD may present with varying degrees of cough, sputum production, dyspnea, wheezing, and chest tightness [8, 9].…”

Section: Introductionmentioning

confidence: 99%

Attenuating immune pathology using a microbial-based intervention in a mouse model of cigarette smoke-induced lung inflammation

Bazett¹,

Biala

Huff

et al. 2017

Respir Res

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BackgroundCigarette smoke exposure is the major risk factor for developing COPD. Presently, available COPD treatments focus on suppressing inflammation and providing bronchodilation. However, these options have varying efficacy in controlling symptoms and do not reverse or limit the progression of COPD. Treatments strategies using bacterial-derived products have shown promise in diseases characterized by inflammation and immune dysfunction. This study investigated for the first time whether a novel immunotherapy produced from inactivated Klebsiella (hereafter referred to as KB) containing all the major Klebsiella macromolecules, could attenuate cigarette smoke exposure-induced immune responses. We hypothesized that KB, by re-directing damaging immune responses, would attenuate cigarette smoke-induced lung inflammation and bronchoalveolar (BAL) cytokine and chemokine production.MethodsKB was administered via a subcutaneous injection prophylactically before initiating a 3-week acute nose-only cigarette smoke exposure protocol. Control mice received placebo injection and room air. Total BAL and differential cell numbers were enumerated. BAL and serum were analysed for 31 cytokines, chemokines, and growth factors. Lung tissue and blood were analysed for Ly6CHI monocytes/macrophages and neutrophils. Body weight and clinical scores were recorded throughout the experiment.ResultsWe demonstrate that KB treatment attenuated cigarette smoke-induced lung inflammation as shown by reductions in levels of BAL IFNγ, CXCL9, CXCL10, CCL5, IL-6, G-CSF, and IL-17. KB additionally attenuated the quantity of BAL lymphocytes and macrophages. In parallel to the attenuation of lung inflammation, KB induced a systemic immune activation with increases in Ly6CHI monocytes/macrophages and neutrophils.ConclusionsThis is the first demonstration that subcutaneous administration of a microbial-based immunotherapy can attenuate cigarette smoke-induced lung inflammation, and modulate BAL lymphocyte and macrophage levels, while inducing a systemic immune activation and mobilization. These data provide a foundation for future studies exploring how KB may be used to either reverse or prevent progression of established emphysema and small airways disease associated with chronic cigarette smoke exposure. The data suggest the intriguing possibility that KB, which stimulates rather than suppresses systemic immune responses, might be a novel means by which the course of COPD pathogenesis may be altered.Electronic supplementary materialThe online version of this article (doi:10.1186/s12931-017-0577-y) contains supplementary material, which is available to authorized users.

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Progression from Asthma to Chronic Obstructive Pulmonary Disease. Is Air Pollution a Risk Factor?

Abstract: Individuals exposed to higher levels of air pollution had nearly threefold greater odds of developing ACOS. Minimizing exposure to high levels of air pollution may decrease the risk of ACOS.

Cited by 120 publications

References 50 publications

Avaliação de impacto à saúde do Programa de Controle de Poluição do Ar por Veículos Automotores no município de São Paulo, Brasil

Avaliação de impacto à saúde do Programa de Controle de Poluição do Ar por Veículos Automotores no município de São Paulo, Brasil

Biomarkers of extracellular matrix turnover are associated with emphysema and eosinophilic-bronchitis in COPD

Attenuating immune pathology using a microbial-based intervention in a mouse model of cigarette smoke-induced lung inflammation

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