PM2.5 induced pulmonary fibrosis in vivo and in vitro

Xu, Zihan; Li, Fulin; Liao, Ziyi; Gao, Sumeng; Li, Hua; Ye, Xiaofei; Wang, Yu; Jiang, Shan; Wang, Ning; Zhou, Dan; Deng, Xiaobei

doi:10.1016/j.ecoenv.2018.12.061

Cited by 98 publications

(65 citation statements)

References 60 publications

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“…Lung physiological section analysis, bronchoalveolar lavage fluid (BALF) analysis, and enzyme‐linked immunosorbent assay are the most widely used methods to analyze the physiological changes in the lung caused by PM 2.5 . Thickening of alveolar wall and infiltration of neutrophils were observed in the lung injury model of PM 2.5 by hemotoxylin and eosin (H&E)‐stained lung physiological sections . Using the BALF method, total cell number, tumor necrosis factor alpha level, interleukin‐6 level, lactate dehydrogenase level, and total protein level in BALF were also found to be higher in the model animals instilled with PM 2.5 solution than in control animals .…”

Section: Introductionmentioning

confidence: 98%

Quantitative evaluation of lung injury caused by PM_2.5 using hyperpolarized gas magnetic resonance

Zhang

et al. 2019

Magnetic Resonance in Med

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Purpose:To demonstrate the feasibility of 129 Xe MR in evaluating the pulmonary physiological changes caused by PM 2.5 in animal models. Methods: Six rats were treated with PM 2.5 solution (16.2 mg/kg) by intratracheal instillation twice a week for 4 weeks, and another six rats treated with normal saline served as the control cohort. Pulmonary function tests, hyperpolarized 129 Xe multi-b diffusion-weighted imaging, and chemical shift saturation recovery MR spectroscopy were performed on all rats, and the pulmonary structure and functional parameters were obtained from hyperpolarized 129 Xe MR data. Additionally, histological analysis was performed on all rats to evaluate alveolar septal thickness. Statistical analysis of all the obtained parameters was performed using unpaired 2-tailed t tests. Results: Compared with the control group, the measured exchange time constant increased from 11.74 ± 2.39 to 14.00 ± 2.84 ms (P < .05), and the septal wall thickness increased from 6.17 ± 0.48 to 6.74 ± 0.52 μm (P < .05) in the PM 2.5 cohort by 129 Xe MR spectroscopy, which correlated well with that obtained using quantitative histology (increased from 5.52 ± 0.32 to 6.20 ± 0.36 μm). Additionally, the mean TP/GAS ratio increased from 0.828 ± 0.115 to 1.019 ± 0.140 in the PM 2.5 cohort (P = .021). Conclusions: Hyperpolarized 129 Xe MR could quantify the changes in gas exchange physiology caused by PM 2.5 , indicating that the technique has the potential to be a useful tool for evaluation of pulmonary injury caused by air pollution in the future. K E Y W O R D Sair pollution, gas exchange, hyperpolarized 129 Xe, lung injury, PM 2.5 570 | ZHANG et Al.

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Section: Introductionmentioning

confidence: 98%

Quantitative evaluation of lung injury caused by PM_2.5 using hyperpolarized gas magnetic resonance

Zhang

et al. 2019

Magnetic Resonance in Med

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“…In recent years, the incidence of pulmonary fibrosis has increased with the increasing severity of air pollution. Epidemiological studies have shown that the increase in the incidence of pulmonary fibrosis is associated with increasing fine particulate matter (PM2.5, aerodynamic diameter ≤ 2.5 μm) levels in the atmosphere 5 . Due to its small diameter, PM2.5 can directly reach the alveoli or even the blood after being inhaled.…”

Section: Introductionmentioning

confidence: 99%

Small GTPase RAB6 deficiency promotes alveolar progenitor cell renewal and attenuates PM2.5-induced lung injury and fibrosis

Yang

Liu

et al. 2020

Cell Death Dis

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Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease characterized by chronic non-specific inflammation of the interstitial lung and extensive deposition of collagen fibers leading to destruction of lung function. Studies have demonstrated that exposure to fine particulate matter (PM2.5) increases the risk of IPF. In order to recover from PM2.5-induced lung injury, alveolar epithelial cells need to be repaired and regenerated to maintain lung function. Type 2 alveolar epithelial cells (AEC2) are stem cells in the adult lung that contribute to the lung repair process through complex signaling. Our previous studies demonstrated that RAB6, a RAS family member lowly expressed in lung cancer, inhibited lung cancer stem cell self-renewal, but it is unclear whether or not and how RAB6 may regulate AEC2 cell proliferation and self-renewal in PM2.5-induced pulmonary fibrosis. Here, we demonstrated that knockout of RAB6 inhibited pulmonary fibrosis, oxidative stress, and AEC2 cell death in PM2.5-injured mice. In addition, knockout of RAB6 decreased Dickkopf 1(DKK1) autocrine and activated proliferation, self-renewal, and wnt/β-catenin signaling of PM2.5-injured AEC2 cells. RAB6 overexpression increased DKK1 autocrine and inhibited proliferation, self-renewal and wnt/β-catenin signaling in AEC2 cells in vitro. Furthermore, DKK1 inhibitors promoted proliferation, self-renewal and wnt/β-catenin signaling of RAB6 overexpressing AEC2 cells, and attenuated PM2.5-induced pulmonary fibrosis in mice. These data establish RAB6 as a regulator of DKK1 autocrine and wnt/β-catenin signal that serves to regulate AEC2 cell proliferation and self-renewal, and suggest a mechanism that RAB6 disruption may promote AEC2 cell proliferation and self-renewal to enhance lung repair following PM2.5 injury.

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“…Studies suggest the existence of a decline in Treg levels and, therefore, an inability to suppress Th1, Th2 and phagocyte responses ( 195 , 196 ). In addition, exposure to PM has been associated with fibrotic events, where IL17 increases synthesis and secretion of collagen in the lung parenchyma ( 197 , 198 ). In addition, it has been described that PM also induces the expression of TGFβ, directly promoting fibroblast differentiation, which could also induce collagen deposition followed by a lower antifibrotic process in the liver ( 199 ).…”

Section: Induction Of An Uncontrolled Inflammatory Process By Air Polmentioning

confidence: 99%

The Challenge by Multiple Environmental and Biological Factors Induce Inflammation in Aging: Their Role in the Promotion of Chronic Disease

et al. 2020

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The aging process is driven by multiple mechanisms that lead to changes in energy production, oxidative stress, homeostatic dysregulation and eventually to loss of functionality and increased disease susceptibility. Most aged individuals develop chronic low-grade inflammation, which is an important risk factor for morbidity, physical and cognitive impairment, frailty, and death. At any age, chronic inflammatory diseases are major causes of morbimortality, affecting up to 5–8% of the population of industrialized countries. Several environmental factors can play an important role for modifying the inflammatory state. Genetics accounts for only a small fraction of chronic-inflammatory diseases, whereas environmental factors appear to participate, either with a causative or a promotional role in 50% to 75% of patients. Several of those changes depend on epigenetic changes that will further modify the individual response to additional stimuli. The interaction between inflammation and the environment offers important insights on aging and health. These conditions, often depending on the individual’s sex, appear to lead to decreased longevity and physical and cognitive decline. In addition to biological factors, the environment is also involved in the generation of psychological and social context leading to stress. Poor psychological environments and other sources of stress also result in increased inflammation. However, the mechanisms underlying the role of environmental and psychosocial factors and nutrition on the regulation of inflammation, and how the response elicited for those factors interact among them, are poorly understood. Whereas certain deleterious environmental factors result in the generation of oxidative stress driven by an increased production of reactive oxygen and nitrogen species, endoplasmic reticulum stress, and inflammation, other factors, including nutrition (polyunsaturated fatty acids) and behavioral factors (exercise) confer protection against inflammation, oxidative and endoplasmic reticulum stress, and thus ameliorate their deleterious effect. Here, we discuss processes and mechanisms of inflammation associated with environmental factors and behavior, their links to sex and gender, and their overall impact on aging.

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PM2.5 induced pulmonary fibrosis in vivo and in vitro

Cited by 98 publications

References 60 publications

Quantitative evaluation of lung injury caused by PM_2.5 using hyperpolarized gas magnetic resonance

Quantitative evaluation of lung injury caused by PM_2.5 using hyperpolarized gas magnetic resonance

Small GTPase RAB6 deficiency promotes alveolar progenitor cell renewal and attenuates PM2.5-induced lung injury and fibrosis

The Challenge by Multiple Environmental and Biological Factors Induce Inflammation in Aging: Their Role in the Promotion of Chronic Disease

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PM2.5 induced pulmonary fibrosis in vivo and in vitro

Cited by 98 publications

References 60 publications

Quantitative evaluation of lung injury caused by PM2.5 using hyperpolarized gas magnetic resonance

Quantitative evaluation of lung injury caused by PM2.5 using hyperpolarized gas magnetic resonance

Small GTPase RAB6 deficiency promotes alveolar progenitor cell renewal and attenuates PM2.5-induced lung injury and fibrosis

The Challenge by Multiple Environmental and Biological Factors Induce Inflammation in Aging: Their Role in the Promotion of Chronic Disease

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Quantitative evaluation of lung injury caused by PM_2.5 using hyperpolarized gas magnetic resonance

Quantitative evaluation of lung injury caused by PM_2.5 using hyperpolarized gas magnetic resonance