Inflammatory marker and aryl hydrocarbon receptor-dependent responses in human macrophages exposed to emissions from biodiesel fuels

Vogel, Christoph F.A.; Kado, Sarah Y.; Kobayashi, Reiko; Liu, Xiaoxue; Wong, Patrick; Na, Kwangsam; Durbin, Thomas D.; Okamoto, Robert A.; Kado, Norman Y.

doi:10.1016/j.chemosphere.2018.12.178

Cited by 32 publications

(20 citation statements)

References 48 publications

(68 reference statements)

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“…Here we report the first supporting evidence for the proposed biological mechanism, describing the presence, in the regulative region of the ACE-2 gene, of putative consensus motifs for the transcription factor AhR. AhR is stimulated by many endogenous and exogenous signals, including environmental pollutants such as PAHs and other noxious molecules contained in PM [ 48 , 49 , 50 ], and different ligands may specifically activate different genes’ subsets [ 51 ]. Besides the primary role in chemical defense by up-regulation of detoxifying xenobiotic enzymes, transforming toxicants into metabolites more easily excreted from the body [ 52 ], AhR acts to regulate microbial defense, organ development, immunity and inflammation [ 53 ].…”

Section: Discussionmentioning

confidence: 98%

Evidence-Based Considerations Exploring Relations between SARS-CoV-2 Pandemic and Air Pollution: Involvement of PM2.5-Mediated Up-Regulation of the Viral Receptor ACE-2

Borro

Girolamo

Gentile

et al. 2020

IJERPH

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The COVID-19/SARS-CoV-2 pandemic struck health, social and economic systems worldwide, and represents an open challenge for scientists —coping with the high inter-individual variability of COVID-19, and for policy makers —coping with the responsibility to understand environmental factors affecting its severity across different geographical areas. Air pollution has been warned of as a modifiable factor contributing to differential SARS-CoV-2 spread but the biological mechanisms underlying the phenomenon are still unknown. Air quality and COVID-19 epidemiological data from 110 Italian provinces were studied by correlation analysis, to evaluate the association between particulate matter (PM)2.5 concentrations and incidence, mortality rate and case fatality risk of COVID-19 in the period 20 February–31 March 2020. Bioinformatic analysis of the DNA sequence encoding the SARS-CoV-2 cell receptor angiotensin-converting enzyme 2 (ACE-2) was performed to identify consensus motifs for transcription factors mediating cellular response to pollutant insult. Positive correlations between PM2.5 levels and the incidence (r = 0.67, p < 0.0001), the mortality rate (r = 0.65, p < 0.0001) and the case fatality rate (r = 0.7, p < 0.0001) of COVID-19 were found. The bioinformatic analysis of the ACE-2 gene identified nine putative consensus motifs for the aryl hydrocarbon receptor (AHR). Our results confirm the supposed link between air pollution and the rate and outcome of SARS-CoV-2 infection and support the hypothesis that pollution-induced over-expression of ACE-2 on human airways may favor SARS-CoV-2 infectivity.

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Section: Discussionmentioning

confidence: 98%

Evidence-Based Considerations Exploring Relations between SARS-CoV-2 Pandemic and Air Pollution: Involvement of PM2.5-Mediated Up-Regulation of the Viral Receptor ACE-2

Borro

Girolamo

Gentile

et al. 2020

IJERPH

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“…As soot and traffic-related particular matter are rich in PAHs, it has been proposed that particle-bound PAHs and their cellular sensor molecule, namely AHR, are causally involved in air pollution-induced skin pigmentation as well [2]. In fact, extracts form airborne particulate matter and diesel exhaust particles have been proven to activate AHR and downstream signaling in various cutaneous and extra-cutaneous test systems [116,117,118].…”

Section: Ahr and Extrinsic Skin Agingmentioning

confidence: 99%

Role of the Aryl Hydrocarbon Receptor in Environmentally Induced Skin Aging and Skin Carcinogenesis

Vogeley

Esser

Tüting

et al. 2019

IJMS

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The skin is constantly exposed to a variety of environmental threats, including solar electromagnetic radiation, microbes, airborne particulate matter, and chemicals. Acute exposure to these environmental factors results in the activation of different signaling pathways that orchestrate adaptive stress responses to maintain cell and tissue homeostasis. Chronic exposure of skin to these factors, however, may lead to the accumulation of damaged macromolecules and loss of cell and tissue integrity, which, over time, may facilitate aging processes and the development of aging-related malignancies. One transcription factor that is expressed in all cutaneous cells and activated by various environmental stressors, including dioxins, polycyclic aromatic hydrocarbons, and ultraviolet radiation, is the aryl hydrocarbon receptor (AHR). By regulating keratinocyte proliferation and differentiation, epidermal barrier function, melanogenesis, and immunity, a certain degree of AHR activity is critical to maintain skin integrity and to adapt to acute stress situations. In contrast, a chronic activation of cutaneous AHR signaling critically contributes to premature aging and the development of neoplasms by affecting metabolism, extracellular matrix remodeling, inflammation, pigmentation, DNA repair, and apoptosis. This article provides an overview of the detrimental effects associated with sustained AHR activity in chronically stressed skin and pinpoints AHR as a promising target for chemoprevention.

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“…Further, COX-2 is a proinflammatory enzyme that has been reported to be involved in inflammatory responses and cytotoxicity after PM stimulation from different sources [52,53]. Previous research has shown that urban dust or diesel exhaust induce IL-8 and COX-2 in an AhR-dependent manner in human U937-derived macrophages [54,55]. AhR is also considered to be an important receptor protein mediating the toxic responses of dioxin-like PAHs [56].…”

Section: Discussionmentioning

confidence: 99%

Effects of Different Components of PM2.5 on the Expression Levels of NF-κB Family Gene mRNA and Inflammatory Molecules in Human Macrophage

Zhu

Zhao

Gao

et al. 2019

IJERPH

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Background: Studies have found that exposure to fine particulate matter with sizes below 2.5 µm (PM2.5) might cause inflammation response via the NF-κB pathway. To date, only a few studies have focused on the toxicity of different components of PM2.5. We aimed to explore the effects of PM2.5 with different components on the expression levels of NF-κB family gene mRNA and inflammatory molecules in human macrophages. Methods: Human monocytic cell line THP-1-derived macrophages were exposed to water-soluble (W-PM2.5), fat-soluble (F-PM2.5), and insoluble (I-PM2.5) PM2.5. The cell survival rate was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The levels of inflammatory molecules were determined by enzyme-linked immunosorbent assay (ELISA), and the relative mRNA levels of the NF-κB family gene were determined by real time PCR. Results: PM2.5 could decrease the cell viability. After exposure to W-PM2.5, the levels of interleukins (IL)-1β and IL-12 p70 significantly increased. After exposure to F-PM2.5, the levels of IL-12 p70 significantly increased. The levels of IL-12 p70 and TNF-α after exposure to I-PM2.5 were significantly higher than that in W- and F-PM2.5 treatment groups. The levels of IL-8, C reactive protein (CRP), and cyclooxygenase (COX)-2 increased only after exposure to I-PM2.5. F-PM2.5 increased the mRNA levels of NF-κB genes, especially NF-κB1 and RelA. Conclusions: PM2.5 can decrease the cell survival rate and up-regulate the expression of NF-κB family gene mRNA and inflammatory molecules. The main toxic components of PM2.5 related to inflammatory response in macrophages were the I-PM2.5.

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Inflammatory marker and aryl hydrocarbon receptor-dependent responses in human macrophages exposed to emissions from biodiesel fuels

Cited by 32 publications

References 48 publications

Evidence-Based Considerations Exploring Relations between SARS-CoV-2 Pandemic and Air Pollution: Involvement of PM2.5-Mediated Up-Regulation of the Viral Receptor ACE-2

Evidence-Based Considerations Exploring Relations between SARS-CoV-2 Pandemic and Air Pollution: Involvement of PM2.5-Mediated Up-Regulation of the Viral Receptor ACE-2

Role of the Aryl Hydrocarbon Receptor in Environmentally Induced Skin Aging and Skin Carcinogenesis

Effects of Different Components of PM2.5 on the Expression Levels of NF-κB Family Gene mRNA and Inflammatory Molecules in Human Macrophage

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