The effect of exposure time and concentration of airborne PM2.5 on lung injury in mice: A transcriptome analysis

Wang, Hongyun; Shen, Xiyue; Liu, Jingli; Wu, Chunyan; Gao, Junling; Zhang, Zezhong; Zhang, Fang; Ding, Wenjun; Lu, Zhigang

doi:10.1016/j.redox.2019.101264

Cited by 55 publications

(34 citation statements)

References 63 publications

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“…To investigate the underlying molecular mechanism of the lung injury posed by PM 2. (Table S3), which was parallel to the previous study about the mice exposed to PM 2.5 collected from Beijing, China [25]. Meanwhile, the top 10 up-and downregulated genes were listed in Table S4.…”

Section: Pm 25 -Induced Changes Of Gene Expression Pro Le In Mice Lungsupporting

confidence: 62%

“…Some evidences have suggested that the adverse effects on lung tissue posed by PM 2.5 maybe associated with the immune and in ammatory response [11,15,32]. Hence, B cell receptor signaling pathway, as the important pathway responsible for immune response [33], enriched by integrated analysis was foreseeable, which was also illuminated by previous study using RNA-sequencing [25]. The transcriptional levels of the target genes involved in this pathway were also signi cantly up-or down-regulated by PM 2.5 .…”

Section: Discussionmentioning

confidence: 90%

“…Recently, this tool has been used to illuminate the associated molecular mechanism of cytotoxicity induced by PM 2.5 [23,24]. There was only one publication about the potential mechanism of lung injury posed by airborne PM 2.5 at Beijing, China using transcriptome analysis [25].…”

Section: Introductionmentioning

confidence: 99%

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Assessment on the lung injury of mice posed by airborne PM2.5 collected from developing area in China and associated molecular mechanisms: from histopathology to integrated transcriptome analysis

Dai

Yang

et al. 2020

Preprint

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Background & aimsSome epidemiological investigations have revealed airborne fine particulate matter (PM2.5) could induce adverse effects on respiratory system of human. However, the experimental evidences of the harmful effect of PM2.5 from mid-scale city in China and associated molecular mechanisms was still scarce. In this study, we aimed to evaluate the adverse effect on the lung system of PM2.5 collected from mid-city of China and elucidate the underlying molecular mechanism through mRNA-seq and microRNA-seq integrated analysis.MethodsWe exposed male Balb/C mice to PM2.5 collected from Baoji city, China for 8 weeks (298.52 ± 25.86 μg/m3) using a whole-body exposure system. Micro-CT and histopathological analyses were performed to determine the morphology and histopathology changes of lung tissues induced by PM2.5. Transcriptome (both mRNA and microRNA) sequencing and the immunohistochemistry assay were performed to reveal the associated underlying mechanisms. The contents of PAHs absorbed in the PM2.5, as well as the pearson correlation index between it and the target genes and microRNA were examined.ResultsObvious lung injury including pulmonary dysfunction, immunological responses, and fibrosis were observed from the PM2.5 exposure group. The content of leucocyte of lung tissue was significantly increased. PM2.5 mainly induced immune pathways including B cell receptor signaling and cell adhesion molecules (CAMs). The expression levels of the associated genes and microRNA were verified using RT-qPCR. The protein expression of CD19, CD81, and PIK3CD involved into B cell receptor signaling significantly increased in exposure group. The concentrations of benzo(a)pyrene (BaP) showed a marked correlationship with the genes and microRNA. ConclusionsPM2.5 from the mid-scale city of China caused adverse effects on lung system of mice, which was much stronger than the mega city, indicating the health risk of the air pollution in the developing area should be paid more attention. The toxicity of PM2.5 may associated with immune system response. This work for the first time provided a new sight into the molecular mechanism of PM2.5 toxicity on lung system using transcriptomics integrated analysis and help further to develop effective measures to prevent air pollution associated lung disease, especially in the developing area in China.

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Section: Pm 25 -Induced Changes Of Gene Expression Pro Le In Mice Lungsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 90%

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Assessment on the lung injury of mice posed by airborne PM2.5 collected from developing area in China and associated molecular mechanisms: from histopathology to integrated transcriptome analysis

Dai

Yang

et al. 2020

Preprint

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“…However, inflammatory effects and major genetic changes appear to be especially dependent on the exposure to high concentrations of PM. One possible explanation is that a prolonged exposure could induce an adaptive response of the inflammatory activation ( 208 ), which may be mediated by the inactivation of the Nrf2 pathway, generating a loss of antioxidant capacity and deregulation of the immune system ( 193 ). The resolution appears to depend on the exposure context.…”

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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“…Poor awareness in smoking habit contributed into smoke-induced lung disease, including COPD, lung cancers and respiratory infections. (17) From the study conducted by (18,19) found that there is a decreasing expression of anioxidant enzymes such as SOD-2, SOD-3, and PRDX4 in mice whose lungs were exposed to PM2.5. This study proving why the SOD-3 level are lower than the IL-6 level.…”

Section: The Difference Of Il-6 and Sod-3 Level In Dyeing And Sizing mentioning

confidence: 99%

The increasing of Interleukin 6 and Superoxide Dismutase 3 nasal wash in textile industry workers exposed by occupational air pollutant

Paramitha¹

2020

IJST

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Background: Occupational air pollution exposure in textiles industry which irritates the respiration system triggers the disturbance of the nasal mucosa. IL-6 is produced by monocytes and macrophages as a response for tissue damage. SOD-3 is extracellular enzymes protected the tissue from free radical and chronic inflammation. Objectives: To know if the occupational air pollution affects the increasing of IL-6 and SOD-3 level on nasal wash. Methods: this study used an analytical observational design with cross-sectional method. It was conducted on 40 male workers of garment industry in Bawen, Semarang, Indonesia. Divided into two groups: the dyeing and sizing area with 20 workers each group. The workers exposed to the occupational air pollutant for 5 years or more. The aquabidest will be injected to subject's nosetril using the 20cc spuit. The nasal wash's sample on the 1.5ml eppendorf tubes will be examined using ELISA method to determine the IL-6 and SOD-3 level. The occupational air pollution indicators will be measured by Envilab Semarang. Findings : The measurements of direct PM10 and PM2.5 in dyeing and sizing area were higher than the regulatory limit. There was a significant difference in the IL-6 level in dyeing and sizing area (p=0,010). There was no significant difference in the SOD-3 level in dyeing and sizing area (p=0,443). There was a positive, moderate and significant correlation between IL-6 and SOD-3 in dyeing and sizing area (r=0.320). Conclusion: The study concluded that the occupational air pollution especially the PM10 and PM2.5 affects the IL-6 and SOD-3 level in the textile industry workers' nasal wash. There is a significant correlation between the IL-6 and SOD-3 level in textile industry workers at dyeing and sizing area. There is a difference in the IL-6 level in dyeing and sizing area. But there is no significant in the SOD-3 level in dyeing and sizing area. The higher occupational air pollution inhaled will be compensated with the higher expression of IL-6 and SOD-3. The higher exposure of PM2.5 in the dyeing area results in the higher level of IL-6 and SOD-3.

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The effect of exposure time and concentration of airborne PM2.5 on lung injury in mice: A transcriptome analysis

Cited by 55 publications

References 63 publications

Assessment on the lung injury of mice posed by airborne PM2.5 collected from developing area in China and associated molecular mechanisms: from histopathology to integrated transcriptome analysis

Assessment on the lung injury of mice posed by airborne PM2.5 collected from developing area in China and associated molecular mechanisms: from histopathology to integrated transcriptome analysis

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

The increasing of Interleukin 6 and Superoxide Dismutase 3 nasal wash in textile industry workers exposed by occupational air pollutant

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