Differential effects of nitro-PAHs and amino-PAHs on cytokine and chemokine responses in human bronchial epithelial BEAS-2B cells

Øvrevik, Johan; Arlt, Volker M.; Øya, Elisabeth; Nagy, Eszter; Mollerup, Steen; Phillips, David H.; Låg, Marit; Holme, Jørn A.

doi:10.1016/j.taap.2009.10.017

Cited by 115 publications

(94 citation statements)

References 69 publications

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“…This is in line with previous findings for one of the most carcinogenic PAHs, B[a]P, which did not induce cytokine responses in the BEAS-2B cells. [19] Thus, the present findings seem to support the previous Fig. 7.…”

Section: Role Of Alkanes Pahs and Their Mildly Polar Derivativessupporting

confidence: 90%

“…These concentrations are about 1000-fold less than those previously used to demonstrate cytokine responses to single PAHs. [19,20] Moreover, these mid-polar (20% DCM in n-hexane) SPE fractions did not induce significant cellular effects (Figs. 5 and 7), and accordingly the content of these groups of compounds did not correlate with the toxicological effects in the linear regression analysis.…”

Section: Role Of Alkanes Pahs and Their Mildly Polar Derivativesmentioning

confidence: 94%

“…[1,18] However, exposure to high concentrations of various single PAHs, as well as nitro-and amino-PAH derivatives, has been reported to induce additional pro-inflammatory responses, both in vivo and in vitro. [19,20] Such effects have been linked to both ligand binding and activation of the aryl hydrocarbon receptor, antagonist properties, as well as to the formation of reactive electrophilic metabolites during the PAH metabolism. [21,22] Although this indicates that PAHs may be important for inflammatory responses, their contribution to the pro-inflammatory effects of DEPs and other combustion particles, to our knowledge, has not yet been clarified.…”

Section: Introductionmentioning

confidence: 99%

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The occurrence of polycyclic aromatic hydrocarbons and their derivatives and the proinflammatory potential of fractionated extracts of diesel exhaust and wood smoke particles

Totlandsdal

Øvrevik

Cochran

et al. 2013

Journal of Environmental Science and Health, Part A

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Exposure to combustion emissions, including diesel engine exhaust and wood smoke particles (DEPs and WSPs), has been associated with inflammatory responses. To investigate the possible role of polycyclic aromatic hydrocarbons (PAHs) and PAH-derivatives, the DEPs and WSPs methanol extracts were fractionated by solid phase extraction (SPE), and the fractions were analyzed for more than ∼120 compounds. The pro-inflammatory effects of the fractionated extracts were characterized by exposure of bronchial epithelial lung cells (BEAS-2B). Both native DEPs and WSPs caused a concentration-dependent increase in IL-6 and IL-8 release and cytotoxicity. This is consistent with the finding of a rather similar total content of PAHs and PAH-derivatives. Yet, the samples differed in specific components, suggesting that different species contribute to the toxicological response in these two types of particles. The majority of the IL-6 release and cytotoxicity was induced upon exposure to the most polar (methanol) SPE fraction of extracts from both samples. In these fractions hydroxy-PAHs, carboxy-PAHs were observed along with nitro-amino-PAHs in DEP. However, the biological effects induced by the polar fractions could not be attributed only to the occurrence of PAH-derivatives. The present findings indicate a need for further characterization of organic extracts, beyond an extensive analysis of commonly suspected PAH and PAH-derivatives.

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Section: Role Of Alkanes Pahs and Their Mildly Polar Derivativessupporting

confidence: 90%

Section: Role Of Alkanes Pahs and Their Mildly Polar Derivativesmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

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The occurrence of polycyclic aromatic hydrocarbons and their derivatives and the proinflammatory potential of fractionated extracts of diesel exhaust and wood smoke particles

Totlandsdal

Øvrevik

Cochran

et al. 2013

Journal of Environmental Science and Health, Part A

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“…BEAS-2B cells, an adenovirus 12-simian virus 40 hybridtransformed human bronchial epithelial cell line, were purchased from American Tissue Type Culture Collection (Rockville, MD, USA) and grown to near-confluence in serum-free LHC-9 medium (Biosource, Camarillo, CA, USA) at 37uC in a humidified atmosphere of 5% CO 2 in air, prior to exposure. Concentrations and incubation times for both the test compounds and inhibitors/ neutralising antibodies were based on previous studies with BEAS-2B or other epithelial lung cells [5,7,18,19,[27][28][29][30][31], or initial screenings in the BEAS-2B cells (data not shown).…”

Section: Reagentsmentioning

confidence: 99%

“…Epithelial cells express a number of pattern-recognition receptors, including Toll-like receptors (TLRs), which recognise conserved pathogen motifs and trigger host responses mediated by various effectors, such as cytokines and chemokines [4]. We have recently shown that increased levels of the neutrophil-selective CXC chemokine ligand (CXCL)8/interleukin (IL)-8 is a dominating pro-inflammatory response to PM and PM components in bronchial epithelial BEAS-2B cells [5][6][7]. Markedly elevated CXCL8 levels, along with neutrophilia, is also characteristic of airway diseases such as chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF) and severe asthma [3,8,9].…”

mentioning

confidence: 99%

TACE/TGF- /EGFR regulates CXCL8 in bronchial epithelial cells exposed to particulate matter components

Øvrevik

Refsnes

Totlandsdal

et al. 2011

European Respiratory Journal

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Airborne particulate matter (PM) may induce or exacerbate neutrophilic airway disease by triggering the release of inflammatory mediators, such as CXC chemokine ligand (CXCL)8, from the airway epithelium. It is still unclear which PM components are driving CXCL8 responses, as most candidates occur at low concentrations in the dusts. We therefore hypothesised that different PM constituents may contribute through common mechanisms to induce CXCL8.Human bronchial epithelial cells (BEAS-2B) were exposed to different PM components (Zn 2+ / Fe 2+ salts, 1-nitropyrene, lipopolysaccharide and diesel exhaust/mineral particles). Gene expression patterns were detected by real-time PCR array. CXCL8 responses were measured by real-time PCR and ELISA. CXCL8 regulation was assessed with a broad inhibitor panel and neutralising antibodies. Epidermal growth factor receptor (EGFR) phosphorylation was examined by immunoprecipitation and Western blotting. Component-induced gene expression was mainly linked to nuclear factor-kB, Ca 2+ /protein kinase C, phospholipase C, low-density lipoprotein and mitogenic signalling. Many inhibitors attenuated CXCL8 release induced by all PM components, but to varying extents. However, EGFR inhibition strongly reduced CXCL8 release induced by all test compounds and selected compounds increased EGFR phosphorylation. Interference with transforming growth factor (TGF)-a or tumour necrosis factor-a-converting enzyme (TACE), which mediates TGF-a ectodomain shedding, also attenuated CXCL8 release. Different PM constituents induced CXCL8 partly through similar signalling pathways but the relative importance of the different pathways varied. However, TACE/TGF-a/EGFR signalling appears to be a convergent pathway regulating innate immune responses of airway epithelial cells upon exposure to multiple airborne pollutants.

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Smoking and COPD and Other Respiratory Diseases

Sussan¹,

Biswal²

2011

Cigarette Smoke Toxicity

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Differential effects of nitro-PAHs and amino-PAHs on cytokine and chemokine responses in human bronchial epithelial BEAS-2B cells

Cited by 115 publications

References 69 publications

The occurrence of polycyclic aromatic hydrocarbons and their derivatives and the proinflammatory potential of fractionated extracts of diesel exhaust and wood smoke particles

The occurrence of polycyclic aromatic hydrocarbons and their derivatives and the proinflammatory potential of fractionated extracts of diesel exhaust and wood smoke particles

TACE/TGF- /EGFR regulates CXCL8 in bronchial epithelial cells exposed to particulate matter components

Smoking and COPD and Other Respiratory Diseases

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