Differential responses of healthy and chronic obstructive pulmonary diseased human bronchial epithelial cells repeatedly exposed to air pollution-derived PM4

Leclercq, B.; Happillon, M.; Anthérieu, Sébastien; Hardy, Emilie; Alleman, L.; Grova, Nathalie; Perdrix, Espéranza; Appenzeller, Brice; Lo-Guidice, Jean-Marc; Coddeville, P.; Garçon, Guillaume

doi:10.1016/j.envpol.2016.08.059

Cited by 62 publications

(42 citation statements)

References 74 publications

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“…Recurrent infections are considered as an important disease‐accelerating factor in COPD, and thus researchers have compared the effect of infection on ALI cultures derived from healthy humans or COPD patients . The alteration of lung epithelial function in PCLS or ALI cultures by toxic inhaled pollutants such as cigarette smoke or diesel exhaust is also an expanding area of research on original human material in the COPD field . Studies range from the observation of acute effects to the investigation of epithelial dedifferentiation and mesenchymal transition …”

Section: Modeled Diseasesmentioning

confidence: 99%

Human Pulmonary 3D Models For Translational Research

Zscheppang

Berg

Hedtrich

et al. 2017

Biotechnology Journal

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Lung diseases belong to the major causes of death worldwide. Recent innovative methodological developments now allow more and more for the use of primary human tissue and cells to model such diseases. In this regard, the review covers bronchial air-liquid interface cultures, precision cut lung slices as well as ex vivo cultures of explanted peripheral lung tissue and de-/re-cellularization models. Diseases such as asthma or infections are discussed and an outlook on further areas for development is given. Overall, the progress in ex vivo modeling by using primary human material could make translational research activities more efficient by simultaneously fostering the mechanistic understanding of human lung diseases while reducing animal usage in biomedical research.

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Section: Modeled Diseasesmentioning

confidence: 99%

Human Pulmonary 3D Models For Translational Research

Zscheppang

Berg

Hedtrich

et al. 2017

Biotechnology Journal

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“…Pulmonary inflammation is enhanced with exposure to air pollutants [19], especially in COPD patients. Compared with healthy human bronchial epithelial cells, COPD bronchial epithelial cells exhibit increased responsiveness to repeated exposure to PM and decreased capacity to metabolize toxins [20]. Additionally, some studies revealed that air pollution may influence systemic inflammation, which can be reflected by serum cytokine levels and white blood cell (WBC) counts [21].…”

Section: Introductionmentioning

confidence: 99%

Lung function and systemic inflammation associated with short-term air pollution exposure in chronic obstructive pulmonary disease patients in Beijing, China

Gao

et al. 2020

Environ Health

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Background: Exposure to air pollution is associated with chronic obstructive pulmonary disease (COPD). However, findings on the effects of air pollution on lung function and systemic inflammation in Chinese COPD patients are inconsistent and scarce. This study aims to evaluate the effects of ambient air pollution on lung function parameters and serum cytokine levels in a COPD cohort in Beijing, China. Methods: We enrolled COPD participants on a rolling basis from December 2015 to September 2017 in Beijing, China. Follow-ups were performed every 3 months for each participant. Serum levels of 20 cytokines were detected every 6 months. Hourly ambient pollutant levels over the same periods were obtained from 35 monitoring stations across Beijing. Geocoded residential addresses of the participants were used to estimate daily mean pollution exposures. A linear mixed-effect model was applied to explore the effects of air pollutants on health in the first-year of follow-up. Results: A total of 84 COPD patients were enrolled at baseline. Of those, 75 COPD patients completed the first-year of follow-up. We found adverse cumulative effects of particulate matter less than 2.5 μm in aerodynamic diameter (PM 2.5), nitrogen dioxide (NO 2), sulfur dioxide (SO 2) and carbon monoxide (CO) on the forced vital capacity % predicted (FVC % pred) in patients with COPD. Further analyses illustrated that among COPD patients, air pollution exposure was associated with reduced levels of serum eotaxin, interleukin 4 (IL-4) and IL-13 and was correlated with increased serum IL-2, IL-12, IL-17A, interferon γ (IFNγ), monocyte displacing protein 1 (MCP-1) and soluble CD40 ligand (sCD40L). Conclusion: Acute exposures to PM 2.5 , NO 2 , SO 2 and CO were associated with a reduction in FVC % pred in COPD patients. Furthermore, short-term exposure to air pollutants increased systemic inflammation in COPD patients; this may be attributed to increased Th1 and Th17 cytokines and decreased Th2 cytokines.

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“…By culturing human primary lung cells at the airliquid interface (ALI), the cells formed a three-dimensional (3D) epithelium closely mimicking the human lung epithelium. 5 This model has provided opportunities to study more complex physiological processes, such as the differential response of COPD and normal bronchial epithelium to air pollution, 6 or the interaction between a pathogen and the epithelium. 7 More recently, organ-on-a-chip technology, the combination of in vitro models with a micro-engineered environment, 8 has facilitated the development of advanced in vitro lung models recreating not only the morphology of the lung epithelium but also its physical movement, which modulates epithelial permeability.…”

Section: Introductionmentioning

confidence: 99%