Metabolomics analysis of a mouse model for chronic exposure to ambient PM2.5

Xu, Yanyi; Wang, Wanjun; Zhou, Ji; Chen, Minjie; Huang, Xingke; Zhu, Yanxia; Xie, Xiaoyun; Li, Weihua; Zhang, Yuhao; Kan, Haidong; Zhao, Ying

doi:10.1016/j.envpol.2019.01.118

Cited by 54 publications

(34 citation statements)

References 43 publications

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“…In the present study, the arti cial climatic environment exposure system (Shanghai-METAS) was used to study the effects of PM 2.5 exposure on kidney damage. This equipment which could maximally simulate "real world" PM 2.5 exposure is the rst comprehensive animal exposure system established in China, and has been effectively used to assess the effects of PM 2.5 exposure on health and diseases development in rodent in several studies (Du et al, 2018;Wang et al, 2018;Xu et al, 2019). Interestingly, the results of this study also con rmed that subchronic exposure to PM 2.5 led to kidney damage in SD rats.…”

Section: Discussionsupporting

confidence: 61%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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Abstract Background: Exposure to airborne fine particulate matter (PM2.5) has been declared to be harmful to human kidney. However, whether activation of the autophagic pathway plays key roles in the nephrotoxicity caused by PM2.5 exposure is still poorly understood. The aim of this study was to explore the mechanism of kidney damage after PM2.5 exposure in vivo and in vitro.Results: In the present study, statistically significant alterations in water intake, urine flow rate and mean blood pressure were observed between the concentrated PM2.5 (PM2.5) group and the filtered air (FA) group. Exposed animals showed severe edema of renal tubular epithelial cells, capillary congestion, reduction of the glomerular urinary space and early pro-fibrotic state. Moreover, significant increases in the levels of early kidney damage markers were observed in the exposed rats and these animals exhibited more apoptosis rate in kidney cells. In addition, PM2.5 exposure activated the autophagic pathway, as evidenced by LC3-I to LC3-II conversion, activation of P62 and beclin-1. All of these effects are in concurrence with the presence of more autophagosomes both in vivo and in vitro after PM2.5 exposure. Conclusions: Taken together, our findings indicated that PM2.5-induced renal function impairment via the activation of the autophagic pathway in renal tubular epithelial cells.

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Section: Discussionsupporting

confidence: 61%

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Huang

Zhou

Liu

et al. 2020

Preprint

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“…Collectively, these data provide a systemic and mechanistic rationale for coordination of the pineal and extrapineal synthesis of melatonin by a common damage‐associated stimulus in a megalopolis. It is well known that air pollution induces lung and systemic inflammatory responses . We confirm that acute exposure to particulate matter (2‐6 hours) induces an increase in circulating proinflammatory cytokines and show a transient increase in the transcription of proinflammatory genes and production of proinflammatory proteins, including TNF, in the pineal gland for the first time.…”

Section: Discussionsupporting

confidence: 79%

“…When animals that were exposed to polluted versus filtered air were compared, a significant reduction in plasma melatonin was detected after 4 hours in a polluted environment. Other authors that maintained animals under a polluted atmosphere for ten months confirmed a reduction in circulating melatonin after this long‐term exposure . Thus, as expected for an acute inflammatory response, a reduction in pineal melatonin synthesis was observed already during the first night.…”

Section: Discussionmentioning

confidence: 52%

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Immune‐pineal axis protects rat lungs exposed to polluted air

Carvalho-Sousa

Pereira

Kinker

et al. 2020

Journal of Pineal Research

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Environmental pollution in the form of particulate matter <2.5 μm (PM2.5) is a major risk factor for diseases such as lung cancer, chronic respiratory infections, and major cardiovascular diseases. Our goal was to show that PM2.5 eliciting a proinflammatory response activates the immune‐pineal axis, reducing the pineal synthesis and increasing the extrapineal synthesis of melatonin. Herein, we report that the exposure of rats to polluted air for 6 hours reduced nocturnal plasma melatonin levels and increased lung melatonin levels. Melatonin synthesis in the lung reduced lipid peroxidation and increased PM2.5 engulfment and cell viability by activating high‐affinity melatonin receptors. Diesel exhaust particles (DEPs) promoted the synthesis of melatonin in a cultured cell line (RAW 264.7 cells) and rat alveolar macrophages via the expression of the gene encoding for AANAT through a mechanism dependent on activation of the NFκB pathway. Expression of the genes encoding AANAT, MT1, and MT2 was negatively correlated with cellular necroptosis, as disclosed by analysis of Gene Expression Omnibus (GEO) microarray data from the human alveolar macrophages of nonsmoking subjects. The enrichment score for antioxidant genes obtained from lung gene expression data (GTEx) was significantly correlated with the levels of AANAT and MT1 but not the MT2 melatonin receptor. Collectively, these data provide a systemic and mechanistic rationale for coordination of the pineal and extrapineal synthesis of melatonin by a standard damage‐associated stimulus, which activates the immune‐pineal axis and provides a new framework for understanding the effects of air pollution on lung diseases.

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“…exposed to filtered air, and the altered metabolites were found to impact amino acid and lipid metabolism pathways. 123 Li et al also reported that human participants exposed to PM 2.5 showed a change in serum metabolites involved in glucose, amino acid, and lipid metabolism. 124 A recent study suggested that house dust may impair sphingolipid metabolism contributing to the development of an asthma phenotype.…”

mentioning

confidence: 96%

Developmental Origins of Health and Disease: Impact of environmental dust exposure in modulating microbiome and its association with non-communicable diseases

Ooi

Tan

Tay

et al. 2020

J Dev Orig Health Dis

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Non-communicable diseases (NCDs) including obesity, diabetes, and allergy are chronic, multi-factorial conditions that are affected by both genetic and environmental factors. Over the last decade, the microbiome has emerged as a possible contributor to the pathogenesis of NCDs. Microbiome profiles were altered in patients with NCDs, and shift in microbial communities was associated with improvement in these health conditions. Since the genetic component of these diseases cannot be altered, the ability to manipulate the microbiome holds great promise for design of novel therapies in the prevention and treatment of NCDs. Together, the Developmental Origins of Health and Disease concept and the microbial hypothesis propose that early life exposure to environmental stimuli will alter the development and composition of the human microbiome, resulting in health consequences. Recent studies indicated that the environment we are exposed to in early life is instrumental in shaping robust immune development, possibly through modulation of the human microbiome (skin, airway, and gut). Despite much research into human microbiome, the origin of their constituent microbiota remains unclear. Dust (also known as particulate matter) is a key determinant of poor air quality in the modern urban environment. It is ubiquitous and serves as a major source and reservoir of microbial communities that modulates the human microbiome, contributing to health and disease. There are evidence that reported significant associations between environmental dust and NCDs. In this review, we will focus on the impact of dust exposure in shaping the human microbiome and its possible contribution to the development of NCDs.

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Metabolomics analysis of a mouse model for chronic exposure to ambient PM2.5

Abstract: Chronic ambient fine particulate matter (PM 2.5) exposure correlates with various adverse health outcomes. Its impact on the circulating metabolome-a comprehensive functional readout of the interaction between an organism's genome and environment-has not however been fully

Cited by 54 publications

References 43 publications

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

PM2.5 exposure induced renal injury via the activation of the autophagic pathway in the rat and HK-2 cell

Immune‐pineal axis protects rat lungs exposed to polluted air

Developmental Origins of Health and Disease: Impact of environmental dust exposure in modulating microbiome and its association with non-communicable diseases

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