Inflammatory responses of urban air PM modulated by chemical composition and different air quality situations in Nanjing, China

Rönkkö, Teemu; Hirvonen, Maija-Riitta; Happo, Mikko S.; Ihantola, Tuukka; Hakkarainen, Henri; Martikainen, Maria-Viola; Gu, Cheng; Wang, Qin’geng; Jokiniemi, Jorma; Komppula, Mika; Jalava, Pasi

doi:10.1016/j.envres.2020.110382

Cited by 17 publications

(5 citation statements)

References 61 publications

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“…The toxicological impact of the aerosol to oxidative stress has been studied using several cellular and acellular methods [12,13], in an attempt to estimate the oxidative and inflammatory activity. The cell-based assays include dichlorofluorescein (DCF), dihydroethidium (DHE), ferricytochrome-c and 4,5-dimethylthiazol-2-yl-2,5-diphenylte-trazolium bromide (MTT), that may significantly demonstrate the cell damage caused by exposure to particles; nevertheless, it cannot provide insights on the mechanism that causes damage, such as oxidative stress [14] and references therein).…”

Section: Introductionmentioning

confidence: 99%

Impact of COVID-19 Lockdown on Oxidative Potential of Particulate Matter: Case of Athens (Greece)

Paraskevopoulou

Bougiatioti

Zarmpas

et al. 2022

Toxics

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This work evaluates the aerosol oxidative potential (OP) and its changes from modified air pollution emissions during the COVID-19 lockdown period in 2020, with the intent of elucidating the contribution of aerosol sources and related components to aerosol OP. For this, daily particulate matter (PM) samples at an urban background site were collected and analyzed with a chemical (acellular) assay based on Dithiothreitol (DTT) during the COVID-19 restriction period in Athens (Greece). The obtained time-series of OP, PM2.5, organic matter (OM) and SO42− of the pre-, post- and lockdown periods were also compared to the data of the same time periods during the years 2017–2019. Even though all traffic-related emissions have been significantly reduced during the lockdown period (by 30%), there is no reduction in water-soluble OP, organics and sulfate concentrations of aerosol during 2020. The results reveal that the decrease in traffic was not sufficient to drive any measurable change on OP, suggesting that other sources—such as biomass burning and secondary aerosol from long-range transport, which remained unchanged during the COVID lockdown—are the main contributors to OP in Athens, Greece.

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Section: Introductionmentioning

confidence: 99%

Impact of COVID-19 Lockdown on Oxidative Potential of Particulate Matter: Case of Athens (Greece)

Paraskevopoulou

Bougiatioti

Zarmpas

et al. 2022

Toxics

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“…The chemical composition of PM could be a composite of polycyclic aromatic hydrocarbons (naphthalene, acenaphthene, pyrene, benzo[k]fluoranthene, and benzo[g,h,i]perylene) and heavy metals (Fe, Zn, Pb, As, Cd, Cr, Cu, and Ni) [ 7 , 8 ]. The toxicity of PM depends on its source, chemical composition, and particle size [ 9 , 10 ]. Recently, we reported that PM 2.5 causes skin damage, skin senescence, and skin inflammation by generating intracellular reactive oxygen species (ROS) [ 11 , 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Hesperidin Protects Human HaCaT Keratinocytes from Particulate Matter 2.5-Induced Apoptosis via the Inhibition of Oxidative Stress and Autophagy

et al. 2022

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Numerous epidemiological studies have reported that particulate matter 2.5 (PM2.5) causes skin aging and skin inflammation and impairs skin homeostasis. Hesperidin, a bioflavonoid that is abundant in citrus species, reportedly has anti-inflammatory properties. In this study, we evaluated the cytoprotective effect of hesperidin against PM2.5-mediated damage in a human skin cell line (HaCaT). Hesperidin reduced PM2.5-induced intracellular reactive oxygen species (ROS) generation and oxidative cellular/organelle damage. PM2.5 increased the proportion of acridine orange-positive cells, levels of autophagy-related proteins, beclin-1 and microtubule-associated protein light chain 3, and apoptosis-related proteins, B-cell lymphoma-2-associated X protein, cleaved caspase-3, and cleaved caspase-9. However, hesperidin ameliorated PM2.5-induced autophagy and apoptosis. PM2.5 promoted cellular apoptosis via mitogen-activated protein kinase (MAPK) activation by promoting the phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, and p38. The MAPK inhibitors U0126, SP600125, and SB203580 along with hesperidin exerted a protective effect against PM2.5-induced cellular apoptosis. Furthermore, hesperidin restored PM2.5-mediated reduction in cell viability via Akt activation; this was also confirmed using LY294002 (a phosphoinositide 3-kinase inhibitor). Overall, hesperidin shows therapeutic potential against PM2.5-induced skin damage by mitigating excessive ROS accumulation, autophagy, and apoptosis.

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“…Human alveolar epithelial cell line A549 (ATCC® CCL-185™, Germany) and THP-1 human monocytes cells (DSMZ ACC 16, Germany) were maintained in DMEM, supplemented with 10% fetal bovine serum (FBS), 2 mM L-glutamine, and 100 U/ml penicillin/streptomycin (all Sigma-Aldrich, USA). For cocultures, monocyte-like THP-1 cells were differentiated into macrophage-like cells with phorbol 12-myristate 13-acetate (PMA) (Sigma-Aldrich) before the experiments, as described in Rönkkö et al [ 15 ].…”

Section: Methodsmentioning

confidence: 99%

“…Membrane Permeability, Oxidative Stress, and Cellular Metabolic Activity. After exposure, cells were detached by trypsinization [15] and analyzed for cell viability, metabolic activity, and production of reactive oxygen species (ROS). Cell viability was analyzed as membrane permeability using propidium iodide (PI), metabolic activity was measured using MTT assay, and the levels of intracellular ROS were measured using 2′, 7′-dichlorofluorescein (DCF) assay as described by Kasurinen et al [16].…”

Section: Pollen and Ligandmentioning

confidence: 99%

Common Pollen Modulate Immune Responses against Viral-Like Challenges in Airway Coculture Model

Tossavainen,

Martikainen,

Loukola

et al. 2023

Journal of Immunology Research

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Recent research indicates that exposure to pollen increases the risk and severity of respiratory infections, while studies also suggest that it may possess a protective function. Our aim was to investigate how exposure to common pollen modifies airway cells’ responses to viral- or bacterial-like challenges and vice versa. Cocultured A549 and THP-1 cells were exposed to three doses of four different pollens (Alnus glutinosa, Betula pendula, Phleum pratense, or Ambrosia artemisiifolia) and subsequently to Toll-like receptor (TLR) ligands mimicking bacterial and viral challenges (TLR3, TLR4, TLR7/8). The stimulation experiment was replicated in reverse order. Toxicological and immunological end points were analyzed. When cells were primed with pollen, especially with grass (P. pratense) or weed (A. artemisiifolia), the ability of cells to secrete cytokines in response to bacterial- and viral-like exposure was decreased. In contrast, cells primed with viral ligand TLR7/8 showed greater cytokine responses against pollen than cells exposed to ligands or pollen alone. Our results suggest that pollen exposure potentially weakens immune reactions to bacterial- or viral-like challenges by modulating cytokine production. They also indicate that TLR7/8-mediated viral challenges could elicit exaggerated immune responses against pollen. Both mechanisms could contribute to the acceleration and complication of infections during the pollen season.

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Inflammatory responses of urban air PM modulated by chemical composition and different air quality situations in Nanjing, China

Cited by 17 publications

References 61 publications

Impact of COVID-19 Lockdown on Oxidative Potential of Particulate Matter: Case of Athens (Greece)

Impact of COVID-19 Lockdown on Oxidative Potential of Particulate Matter: Case of Athens (Greece)

Hesperidin Protects Human HaCaT Keratinocytes from Particulate Matter 2.5-Induced Apoptosis via the Inhibition of Oxidative Stress and Autophagy

Common Pollen Modulate Immune Responses against Viral-Like Challenges in Airway Coculture Model

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