Exposure to ultrafine particulate matter induces NF-κβ mediated epigenetic modifications

Bhargava, Arpit; Shukla, Anushi; Bunkar, Neha; Shandilya, Ruchita; Lodhi, Lalit; Kumari, Roshani; Gupta, P. K.; Rahman, Akhlaqur; Chaudhury, Koel; Tiwari, Rajnarayan R; Goryacheva, Irina Yu.; Mishra, Pradyumna Kumar

doi:10.1016/j.envpol.2019.05.065

Cited by 62 publications

(32 citation statements)

References 77 publications

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“…The response of a cell to a reactive oxygen-rich environment often involves the activation of numerous intracellular signaling pathways, which cause transcriptional changes and allow the cells to respond appropriately to the perceived oxidative stress 13,14 . Nuclear factor-κB (NF-κB), activation protein-1 (AP-1), nuclear factor erythroid 2 related factor 2 (Nrf2), and CREB-binding proteins (CBPs) are regulated and influenced by redox status and have been implicated in the transcriptional regulation of a wide range of genes that are involved in oxidative stress and cellular response mechanisms 23 .…”

Section: Reactive Oxygen Species and Oxidative Stressmentioning

confidence: 99%

“…Redox status in the nucleus affects histone acetylation and deacetylation status, which regulates inflammatory gene expression by activation of redox-sensitive transcription factors 25 . NF-κB is activated in epithelial cells and inflammatory cells during oxidative stress, leading to the upregulation of many proinflammatory genes 23 . NF-κB is a protein heterodimer that consists of p65 and p50 subunits.…”

Section: Reactive Oxygen Species and Oxidative Stressmentioning

confidence: 99%

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Mechanisms of ultrafine particle-induced respiratory health effects

2020

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Particulate matter (PM) is the principal component of air pollution. PM includes a range of particle sizes, such as coarse, fine, and ultrafine particles. Particles that are <100 nm in diameter are defined as ultrafine particles (UFPs). UFPs are found to a large extent in urban air as both singlet and aggregated particles. UFPs are classified into two major categories based on their source. Typically, UFPs are incidentally generated in the environment, often as byproducts of fossil fuel combustion, condensation of semivolatile substances or industrial emissions, whereas nanoparticles are manufactured through controlled engineering processes. The primary exposure mechanism of PM is inhalation. Inhalation of PM exacerbates respiratory symptoms in patients with chronic airway diseases, but the mechanisms underlying this response remain unclear. This review offers insights into the mechanisms by which particles, including UFPs, influence airway inflammation and discusses several mechanisms that may explain the relationship between particulate air pollutants and human health, particularly respiratory health. Understanding the mechanisms of PMmediated lung injury will enhance efforts to protect at-risk individuals from the harmful health effects of air pollutants.

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Section: Reactive Oxygen Species and Oxidative Stressmentioning

confidence: 99%

Section: Reactive Oxygen Species and Oxidative Stressmentioning

confidence: 99%

Mechanisms of ultrafine particle-induced respiratory health effects

2020

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“…Fine and ultra ne PMs have been reported to induce lung diseases through generation of ROS and oxidative stress as well as activation of innate and adaptive immunity, leading to cell barrier and tissue damage (22,23). Several known promoters of in ammatory response, such as nuclear factor-κB (NF-κB), activation protein-1 (AP-1), nuclear factor erythroid 2 related factor 2 (Nrf2), and CREB-binding proteins (CBPs), are activated by oxidative stress (24)(25)(26). In our study, we observed signi cantly higher levels of oxidative stress and IL-6 in together with up-regulation of in ammation-related pathways including acute phase response and complement system in rats exposed to PM 1 for 3 months.…”

Section: Discussionmentioning

confidence: 99%

Prolonged Exposure to Traffic-related Particulate Matter Showed Distinct Molecular Mechanisms of Lung Injury in Rats

Jheng¹,

Putri²,

Chuang³

et al. 2020

Preprint

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Background: Exposure to particulate matter (PM) pollution has direct impacts on the respiratory organs, yet the molecular alterations underlying PM-induced pulmonary injury remain unclear. In this study, we investigated the effect of PM on lung tissues of SD rats with whole-body exposure to traffic-related PM1 (< 1 mm in aerodynamic diameter) pollutants and compared it with rats exposed to high-efficiency particulate air-filtered gaseous pollutants and clean air control for 3 and 6 months. Lung function and histological examinations as well as quantitative proteomics analysis and functional validation were performed. Results: The rats in 6-month PM1-exposed group showed significant decline in lung function by decreased forced expiratory flow and forced expiratory volume, but the histological analysis revealed an earlier lung damage evidenced by increased congestion and macrophage infiltration in 3-month PM1-exposed rat lungs. The lung tissue proteomics analysis identified 2,673 proteins which highlighted dysregulations on proteins involved in oxidative stress, cellular metabolisms, calcium signaling, inflammatory responses, and actin dynamics. The presence of fine particles specifically enhanced the oxidative stress and inflammatory reactions under sub-chronic exposure of traffic-related PM1 and suppressed the glucose metabolism and actin cytoskeleton signaling which might lead to repair failure and thus lung function decline after chronic exposure of traffic-related PM1. A detailed pathogenic mechanism was proposed to depict the temporal and dynamic molecular regulations associated with PM1-induced lung injury.Conclusion: Our study explored the earlier lung injury prior to lung function decline and proposed potential molecular features for traffic-related PM1-induced lung injury.

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“…In terms of the molecular and cellular mechanism induced by pollutants, PM and SOx can generate ROS, inducing oxidative stress, together with mitochondrial dysfunction and the consequent energy deprivation ( 185 – 187 ). As a direct consequence, NFκB and MAPK inflammatory pathways are activated, triggering an innate immune activation ( 188 , 189 ). Despite the attempts to resolve the inflammatory event, the outcome appears to be an imbalance in lymphocyte homeostasis and immune system dysregulation, with inhibition of Th1 and Treg lymphocytes ( 190 ).…”

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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Exposure to ultrafine particulate matter induces NF-κβ mediated epigenetic modifications

Cited by 62 publications

References 77 publications

Mechanisms of ultrafine particle-induced respiratory health effects

Mechanisms of ultrafine particle-induced respiratory health effects

Prolonged Exposure to Traffic-related Particulate Matter Showed Distinct Molecular Mechanisms of Lung Injury in Rats

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

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