Exposure to Ambient Particulate Matter Induced COPD in a Rat Model and a Description of the Underlying Mechanism

He, Fang; Liao, Baoling; Pu, Jinding; Li, Chenglong; Zheng, Mengning; Huang, Lingmei; Zhou, Yumin; Zhao, Dongxing; Li, Bing; Ran, Pixin

doi:10.1038/srep45666

Cited by 69 publications

(83 citation statements)

References 37 publications

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“…As shown by Kim et al, diesel exhaust particles, a major component of PM2.5, increase lung fibrosis, goblet cell hyperplasia, and inflammation in a mouse model . He et al found that chronic exposure to PM2.5 induced pronounced lower airway remodeling, mucus overproduction, and inflammatory cell infiltration in a rat model . Consistent with these findings, in the present study, PM2.5 exposure induced a marked increase in goblet cell hyperplasia and collagen deposition in the nasal mucosa that was significantly enhanced in CRS rabbits, suggesting that PM2.5 acted as an adjuvant in exacerbating remodeling changes in CRS.…”

Section: Discussionsupporting

confidence: 91%

Effects of PM2.5 on mucus secretion and tissue remodeling in a rabbit model of chronic rhinosinusitis

Zhao

Dong

Deng

et al. 2018

Int Forum Allergy Rhinol

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Section: Discussionsupporting

confidence: 91%

Effects of PM2.5 on mucus secretion and tissue remodeling in a rabbit model of chronic rhinosinusitis

Zhao

Dong

Deng

et al. 2018

Int Forum Allergy Rhinol

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“…Until now, reports on MVE exposure to establish COPD models have not been widely recognized, and most of them indicated that the MVE exposure can decrease lung function and increase airway inflammation (He et al, 2017;Wright et al, 2005). However, it is still unknown exactly how the pulmonary vascular changes develop over time and whether these changes are related to the lung damage and airway inflammation.…”

Section: • What Is the Central Question Of This Study?mentioning

confidence: 99%

“…The environment conditions of the MVE exposure system and the changes in the concentration of PM and gas were according to the previously published protocol (He et al, 2017). The concentration of PM in the vehicle exhaust gas-exposed system measured using the TSI8533 particle analyser (TSI Inc., Shoreview, MN, USA) was as follows.…”

Section: Animals and Mve Exposurementioning

confidence: 99%

Establishment and evaluation of chronic obstructive pulmonary disease model by chronic exposure to motor vehicle exhaust combined with lipopolysaccharide instillation

Shu

Yang

et al. 2018

Experimental Physiology

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Although it is well established that motor vehicle exhaust (MVE) has a close association with the occurrence and exacerbation of chronic obstructive pulmonary disease (COPD), very little is known about the combined effects of MVE and intermittent or chronic subclinical inflammation on COPD pathogenesis. Therefore, given the crucial role of inflammation in the development of COPD, we wanted to establish an animal model of COPD using both MVE exposure and airway inflammation, which could mimic the clinical pathological changes observed in COPD patients and greatly benefit the study of the molecular mechanisms of COPD. In the present study, we report that mice undergoing chronic exposure to MVE and intratracheal instillation of lipopolysaccharide (LPS) successfully established COPD, as characterized by persistent air flow limitation, airway inflammation, inflammatory cytokine production, emphysema and small airway remodelling. Moreover, the mice showed significant changes in ventricular and vascular pathology, including an increase in right ventricular pressure, right ventricular hypertrophy and remodelling of pulmonary arterial walls. We have thus established a new mouse COPD model by combining chronic MVE exposure with early intratracheal instillation of LPS, which will allow us to study the relationship between air pollution and the development of COPD and to investigate the underlying molecular mechanisms.

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“…Liu et al, 2017). Study showed that in PM-induced rat model, many pathogenesis that related to COPD were activated, including pulmonary inflammation measured by bronchoalveolar lavage fluid (BALF) inflammatory cell counts, increased inflammatory cytokine expression in BALF and serum, emphysematous changes, airway remodeling and mucus metaplasia (He et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Hydrogen Sulfide Attenuates Particulate Matter-Induced Emphysema and Airway Inflammation Through Nrf2-Dependent Manner

Jia

Sun

et al. 2020

Front. Pharmacol.

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Purpose: To investigate whether hydrogen sulfide provide protective effects on atmosphere particulate matter (PM)-induced emphysema and airway inflammation and its mechanism.Methods: Wild type C57BL/6 and Nrf2 knockout mice were exposed to PM (200 µg per mouse). Hydrogen sulfide or propargylglycine were administered by intraperitoneal injection respectively 30 min before PM exposure, mice were anesthetized 29th day after administration. Mice emphysema, airway inflammation, and oxidative stress were evaluated, the expression of NLRP3, active caspase-1, and active caspase-3 were detected. Alveolar epithelial A549 cells line were transfected with control small interfering RNA (siRNA) or Nrf2 siRNA and then incubated with or without hydrogen sulfide for 30 min before exposed to fine particulate matter for 24 h, cell viability, terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling (TUNEL) assay, the secretion of interleukin (IL)-1b, ASC speck formation, the expression level of NLRP3, active caspase-1, and active caspase-3 were measured. Results: PM significantly increased mice emphysema and airway inflammation measured by mean linear intercept, alveolar destroy index and total cell, neutrophil counts, cytokines IL-6, tumor necrosis factor (TNF)-a, CXCL1, IL-1b in bronchoalveolar lavage fluid. PMinduced mice emphysema and airway inflammation was greatly attenuated by hydrogen sulfide, while propargylglycine aggravated that. PM-induced oxidative stress was reduced by hydrogen sulfide as evaluated by 8-OHdG concentrations in lung tissues. The expression of NLRP3, active caspase-1, and active caspase-3 enhanced by PM were also downregulated by hydrogen sulfide in mice lung. The protective effect of hydrogen sulfide on emphysema, airway inflammation, inhibiting oxidative stress, NLRP3 inflammasome formation, and anti-apoptosis was inhibited by Nrf2 knockout in mice. Similarly, hydrogen Frontiers in Pharmacology | www.frontiersin.org

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Exposure to Ambient Particulate Matter Induced COPD in a Rat Model and a Description of the Underlying Mechanism

Cited by 69 publications

References 37 publications

Effects of PM2.5 on mucus secretion and tissue remodeling in a rabbit model of chronic rhinosinusitis

Effects of PM2.5 on mucus secretion and tissue remodeling in a rabbit model of chronic rhinosinusitis

Establishment and evaluation of chronic obstructive pulmonary disease model by chronic exposure to motor vehicle exhaust combined with lipopolysaccharide instillation

Hydrogen Sulfide Attenuates Particulate Matter-Induced Emphysema and Airway Inflammation Through Nrf2-Dependent Manner

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