Cytokine responses induced by diesel exhaust particles are suppressed by PAR-2 silencing and antioxidant treatment, and driven by polar and non-polar soluble constituents

Bach, Nicolai S.; Bølling, Anette Kocbach; Brinchmann, Bendik Christian; Totlandsdal, Annike I.; Skuland, Tonje; Holme, Jørn A.; Låg, Marit; Schwarze, Per E.; Øvrevik, Johan

doi:10.1016/j.toxlet.2015.07.002

Cited by 19 publications

(18 citation statements)

References 55 publications

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“…The explanation is unclear, but it may be that ROS modulation of Si50‐induced cytokine responses involves translational or post‐translational mechanisms. In resemblance, in our previous study, the suppressive effects of antioxidant treatment (NAC, thiourea) on diesel exhaust particle‐induced IL‐6 and CXCL8 responses in BEAS‐2B cells were also much more pronounced on cytokine release compared to the effects on gene expression . Interestingly, it has been reported a role for NADPH‐induced ROS formation in secretion of IL‐1β from neutrophils .…”

Section: Discussionsupporting

confidence: 76%

“…In resemblance, in our previous study, the suppressive effects of antioxidant treatment (NAC, thiourea) on diesel exhaust particle-induced IL-6 and CXCL8 responses in BEAS-2B cells were also much more pronounced on cytokine release compared to the effects on gene expression. 52 Interestingly, it has been reported a role for NADPH-induced ROS formation in secretion of IL-1β from neutrophils. 53 A possibility is therefore that the transport of cytokines across the plasma membrane in BEAS-2B cells is dependent on redox-regulated processes.…”

Section: Discussionmentioning

confidence: 99%

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Concentration‐dependent cytokine responses of silica nanoparticles and role of ROS in human lung epithelial cells

Refsnes

Skuland

Lilleaas

et al. 2019

Basic Clin Pharma Tox

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Reactive oxygen species (ROS) is regarded as a critical denominator in nanoparticle toxicology and inflammation. Previously, we have shown that silica nanoparticles sized 50 nm (Si50) induce release of CXCL8 and IL‐6 from BEAS‐2B cells, via mechanisms involving NFκB, p38 MAP kinase and TGF‐α‐activated EGF receptor. In the present study, the role of ROS‐mediated mechanisms in the concentration‐dependent Si50 induction of CXCL8 and IL‐6 responses was examined. Si50 (200 µg/mL) induced a time‐dependent ROS formation and a postponed increase in expression of haem oxygenase (HO‐1) mRNA and protein. Pre‐treatment with the ROS inhibitors N‐acetyl cysteine (NAC) and diphenyleneiodonium (DPI) partially attenuated CXCL8 and IL‐6 responses to 200 µg/mL, but not to 100 µg/mL Si50. The release of TGF‐α induced by Si50 (200 µg/mL) was significantly reduced by NAC, but not by DPI nor siRNA against NADPH oxidase DUOX‐1 (siDUOX‐1). Furthermore, siDUOX‐1 reduced Si50‐induced CXCL8, but not IL‐6. Both p38 and p65 phosphorylations were inhibited by siDUOX‐1, but for NAC only p65 phosphorylation reached a significant reduction. Neither NAC nor DPI reduced Si50‐induced CXCL8 and IL‐6 gene expressions. In conclusion, Si50‐induced CXCL8 and IL‐6 involved both ROS‐dependent and ROS‐independent mechanisms. Notably, the role of ROS seemed restricted to effects of higher concentrations of Si50 and not mediated via the gene expression.

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Section: Discussionsupporting

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Concentration‐dependent cytokine responses of silica nanoparticles and role of ROS in human lung epithelial cells

Refsnes

Skuland

Lilleaas

et al. 2019

Basic Clin Pharma Tox

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“…MMP‐1 is involved in the breakdown of extracellular matrix and is associated with COPD and associated with cancer growth and metastasis . In extension of this, studies from our laboratory show that PAR‐2 silencing suppressed DEP‐induced IL‐6 responses in BEAS‐2B cells . Also in this case, the effect was linked to components in the organic fraction (fig.…”

Section: Interaction With the Plasma Membrane Cell Surface Receptorsmentioning

confidence: 59%

Triggering Mechanisms and Inflammatory Effects of Combustion Exhaust Particles with Implication for Carcinogenesis

Øvrevik

Refsnes

Låg

et al. 2017

Basic Clin Pharma Tox

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A number of biological responses may contribute to the carcinogenic effects of combustion-derived particulate matter (CPM). Here, we focus on mechanisms that trigger CPM-induced pro-inflammatory responses. Inflammation has both genotoxic and non-genotoxic implications and is considered to play a central role in development of various health outcome associated with CPM exposure, including cancer. Chronic, low-grade inflammation may cause DNA damage through a persistent increased level of reactive oxygen species (ROS) produced and released by activated immune cells. Moreover, a number of pro-inflammatory cytokines and chemokines display mitogenic, motogenic, morphogenic and/or angiogenic properties and may therefore contribute to tumour growth and metastasis. The key triggering events involved in activation of pro-inflammatory responses by CPM and soluble CPM components can be categorized into (i) formation of ROS and oxidative stress, (ii) interaction with the lipid layer of cellular membranes, (iii) activation of receptors, ion channels and transporters on the cell surface and (iv) interactions with intracellular molecular targets including receptors such as the aryl hydrocarbon receptor (AhR). In particular, we will elucidate the effects of diesel exhaust particles (DEP) using human lung epithelial cells as a model system.

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“…PM on the filter was extracted into methanol. Further, methanol was purged and samples were reconstituted with DMSO [67, 68]. Samples were pooled and used for further experiments.…”

Section: Methodsmentioning

confidence: 99%

Imperative role of particulate matter in innate immunity during RNA virus infection

Mishra

Pandikannan

Gangamma

et al. 2020

Preprint

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25Sensing of pathogens by specialized receptors is the hallmark of the innate immune response. 26Innate immune response also mounts a defense response against various allergens and pollutants 27 including particulate matter present in the atmosphere. Air pollution has been included as the top 28 threat to global health declared by WHO which aims to cover more than three billion people against 29 health emergencies from 2019-2023. Particulate matter (PM), one of the major components of air 30 pollution, is a significant risk factor for many human diseases and its adverse effects include 31 morbidity and premature deaths throughout the world. Several clinical and epidemiological studies 32 have identified a key link between the PM composition and the prevalence of respiratory and 33 inflammatory disorders. However, the underlying molecular mechanism is not well understood. 34Here, we investigated the influence of air pollutant, PM10 during RNA virus infections using highly 35 pathogenic avian influenza (HPAI). We thus characterized the transcriptomic profile of lung 36 epithelial cell line, A549 treated with PM10 prior to infection with (HPAI) H5N1 influenza virus, 37 which is known to severely affect the lung and cause respiratory damage. We found that PM10 38 regulates virus infectivity and enhances overall pathogenic burden in the lung cells. Additionally, 39 the transcriptomic profile highlights the connection of host factors related to various metabolic 40 pathways and immune responses which were dysregulated during virus infection. Overall our 41 findings suggest a strong link between the prevalence of respiratory illness and the air quality. 42 43 44 45 Keywords: Particulate Matter (PM10), Virus Infection, Infectious Disease, Innate Immunity and 46 Metabolic Pathways-Related Genes. 47India and associated health concerns in term of occurrence of disease [14][15][16][17][18][19]. Although, most of 65 the studies were based on the epidemiological data and cross-sectional studies, there were few 66 studies about involvement of PM in respiratory diseases [20][21][22], asthma [23], cancer [24-27], 67 tuberculosis [28, 29] . It has been known that PM can induce innate immunity and can change the 68 level of cytokines, upon its exposure to the airways of humans [30][31][32][33]. PM were readily associated 69 with respiratory infections such as chronic obstructive pulmonary disease (COPD) [34][35][36][37] and it 70 is also reported to be associated with the respiratory syncytial virus (RSV) and influenza virus 71infections. [38][39][40][41]. Yet these studies are limited to epidemiological, cross -sectional studies [22, 72 42-44]. 73Here, we isolated and characterized PM10 from a heavily industrialized city Bengaluru, India and 74 checked its effect on RNA virus infection. We observed and concluded that PM10 hijacks the innate 75 immune system upon viral infection and significantly enhanced the viral replication of the RNA 76 viruses like new-castle disease virus (NDV), influenza virus -H1N1 (PR8) and H5N1. By 77...

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Cytokine responses induced by diesel exhaust particles are suppressed by PAR-2 silencing and antioxidant treatment, and driven by polar and non-polar soluble constituents

Cited by 19 publications

References 55 publications

Concentration‐dependent cytokine responses of silica nanoparticles and role of ROS in human lung epithelial cells

Concentration‐dependent cytokine responses of silica nanoparticles and role of ROS in human lung epithelial cells

Triggering Mechanisms and Inflammatory Effects of Combustion Exhaust Particles with Implication for Carcinogenesis

Imperative role of particulate matter in innate immunity during RNA virus infection

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