Gene expression profiling of human bronchial epithelial cells exposed to fine particulate matter (PM 2.5 ) from biomass combustion

Popadić, Désirée; Heßelbach, Katharina; Richter-Brockmann, Sigrid; Kim, Gwang-Jin; Flemming, Stephan; Schmidt‐Heck, Wolfgang; Häupl, Thomas; Bonin, Marc; Dornhof, Regina; Achten, Christine; Günther, Stefan; Humar, Matjaž; Merfort, Irmgard

doi:10.1016/j.taap.2018.03.024

Cited by 7 publications

(10 citation statements)

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“…Molecular investigations using biofuel combustion particles are mainly focused on toxicity and inflammation [11][12][13]. Previously we investigated the methylome and gene expression profile of PM 2.5 -exposed BEAS-2B bronchial epithelial cells, revealing multiple putative pathways for cancer development and progression, and indicating susceptibility to microbial infections or other pulmonary associated diseases [14,15]. We also observed the induction of a stress response that preserved cellular integrity during long-term exposure to PM 2.…”

Section: Introductionmentioning

confidence: 84%

“…The collection, characterization, and intracellular distribution of PM 2.5 have been described previously [15,16]. Briefly, particles from biomass combustion were obtained from a biomass powerplant (Bürger Energie St. Peter eG, St. Peter, Schwarzwald, Germany), which exclusively combusts chips of soft wood (mainly spruce) from the local forest.…”

Section: Ambient Particulate Matter (Pm 25 )mentioning

confidence: 99%

“…The collected bulk fly ash was size-fractionated by a cyclone, and particles of the size fraction with an aerodynamic cut-off diameter of <2.5 µm were used for biological assays. The detailed characterization of the PM 2.5 fraction is described in our previous studies [15,16]. Lipopolysaccharide content was determined by a limulus amebocyte lysate (LAL) test as described elsewhere [35].…”

Section: Ambient Particulate Matter (Pm 25 )mentioning

confidence: 99%

“…The Affymetrix HG-U133 Plus 2.0 oligonucleotide microarrays (Affymetrix, Santa Clara, CA, USA) were used and analyzed as described elsewhere [14,15]. Data have been deposited at https://www.ncbi.…”

Section: Microarray Analysismentioning

confidence: 99%

“…Lipopolysaccharide levels were below the detection limit of the limulus amebocyte lysate (LAL) test (>0.03 EU/mL or 0.3 EU/mg). Polycyclic aromatic hydrocarbon (PAH) analysis was performed previously by GC-APLI-MS and revealed a content of 349.83 µg/kg PM 2.5 , with fluoranthene, pyrene, phenanthrene, and retene presenting the main compounds (Table S2) [15].…”

Section: Characterization Of Pm 25 From Biomass Combustionmentioning

confidence: 99%

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Particulate Matter (PM2.5) from Biomass Combustion Induces an Anti-Oxidative Response and Cancer Drug Resistance in Human Bronchial Epithelial BEAS-2B Cells

Merk

Heßelbach

Osipova

et al. 2020

IJERPH

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Nearly half of the world’s population relies on combustion of solid biofuels to cover fundamental energy demands. Epidemiologic data demonstrate that particularly long-term emissions adversely affect human health. However, pathological molecular mechanisms are insufficiently characterized. Here we demonstrate that long-term exposure to fine particulate matter (PM2.5) from biomass combustion had no impact on cellular viability and proliferation but increased intracellular reactive oxygen species (ROS) levels in bronchial epithelial BEAS-2B cells. Exposure to PM2.5 induced the nuclear factor erythroid 2-related factor 2 (Nrf2) and mediated an anti-oxidative response, including enhanced levels of intracellular glutathione (GSH) and nuclear accumulation of heme oxygenase-1 (HO-1). Activation of Nrf2 was promoted by the c-Jun N-terminal kinase JNK1/2, but not p38 or Akt, which were also induced by PM2.5. Furthermore, cells exposed to PM2.5 acquired chemoresistance to doxorubicin, which was associated with inhibition of apoptosis and elevated levels of GSH in these cells. Our findings propose that exposure to PM2.5 induces molecular defense mechanisms, which prevent cellular damage and may thus explain the initially relative rare complications associated with PM2.5. However, consistent induction of pro-survival pathways may also promote the progression of diseases. Environmental conditions inducing anti-oxidative responses may have the potential to promote a chemoresistant cellular phenotype.

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