Dataset Information

Particulate Matter 2.5 Causes Deficiency in Barrier Integrity in Human Nasal Epithelial Cells.

ABSTRACT:

Purpose

The effect of air pollution-related particulate matter (PM) on epithelial barrier function and tight junction (TJ) expression in human nasal mucosa has not been studied to date. This study therefore aimed to assess the direct impact of PM with an aerodynamic diameter less than 2.5 ? (PM2.5) on the barrier function and TJ molecular expression of human nasal epithelial cells.

Methods

Air-liquid interface cultures were established with epithelial cells derived from noninflammatory nasal mucosal tissue collected from patients undergoing paranasal sinus surgery. Confluent cultures were exposed to 50 or 100 ?g/mL PM2.5 for up to 72 hours, and assessed for 1) epithelial barrier integrity as measured by transepithelial resistance (TER) and permeability of fluorescein isothiocyanate (FITC) 4 kDa; 2) expression of TJs using real-time quantitative polymerase chain reaction and immunofluorescence staining, and 3) proinflammatory cytokines by luminometric bead array or enzyme-linked immunosorbent assay.

Results

Compared to control medium, 50 and/or 100 ?g/mL PM2.5-treatment 1) significantly decreased TER and increased FITC permeability, which could not be restored by budesonide pretreatment; 2) significantly decreased the expression of claudin-1 messenger RNA, claudin-1, occludin and ZO-1 protein; and 3) significantly increased production of the cytokines interleukin-8, TIMP metallopeptidase inhibitor 1 and thymic stromal lymphopoietin.

Conclusions

Exposure to PM2.5 may lead to loss of barrier function in human nasal epithelium through decreased expression of TJ proteins and increased release of proinflammatory cytokines. These results suggest an important mechanism of susceptibility to rhinitis and rhinosinusitis in highly PM2.5-polluted areas.

SUBMITTER: Xian M

PROVIDER: S-EPMC6875480 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Publications

Particulate Matter 2.5 Causes Deficiency in Barrier Integrity in Human Nasal Epithelial Cells.

Xian Mu M Ma Siyuan S Wang Kuiji K Lou Hongfei H Wang Yang Y Zhang Luo L Wang Chengshuo C Akdis Cezmi A CA

Allergy, asthma & immunology research 20200101 1

<h4>Purpose</h4>The effect of air pollution-related particulate matter (PM) on epithelial barrier function and tight junction (TJ) expression in human nasal mucosa has not been studied to date. This study therefore aimed to assess the direct impact of PM with an aerodynamic diameter less than 2.5 μ (PM2.5) on the barrier function and TJ molecular expression of human nasal epithelial cells.<h4>Methods</h4>Air-liquid interface cultures were established with epithelial cells derived from noninflamm ...[more]

PMID: 31743964

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Project description:BackgroundEosinophilic chronic rhinitis with nasal polyps (eos-CRSwNP) is a subtype of nasal polyps (NPs) characterized by severe type-2 inflammation and defective epithelial barrier function. The epithelial barrier plays important roles in the pathogenesis of NPs and type-2 inflammation. Particular matter 2.5 (PM2.5) are fine particles with a diameter less than 2.5 μm, containing a mixture of different components. Here, we investigated the impact of PM2.5 on the barrier function of the eos-CRSwNP epithelium and explored the reparative function of budesonide.MethodsSamples from noninflammatory nasal mucosa and eos-CRSwNP were collected to establish an in vitro air-liquid interface cultured model. The cells were exposed to PM2.5 at 50 or 100 µg/ml intermittently for 72 h, with or without budesonide pretreatment. Barrier function and tight junction (TJ) expression were reflected by measuring transepithelial resistance (TER), paracellular flux permeability of fluorescein isothiocyanate-labeled 4-kDa dextran, quantitative real-time polymerase chain reaction (qPCR), and immunofluorescence staining of TJ proteins. Cytokine expression was measured by qPCR and enzyme-linked immunosorbent assay or Luminex.ResultsPM2.5 increased paracellular flux and downregulated TJ protein expression (zona occuldens-1, occludin, and claudin-1), but did not change TER. These changes could be partially restored by budesonide treatment. Interleukin (IL)-8, IL-10, IL-1α, and tissue inhibitor of metalloproteinase (TIMP)-1 concentrations were significantly increased in the culture medium of cells exposed to PM2.5, and budesonide significantly reduced the changes in IL-8, IL-1α, and TIMP-1.ConclusionPM2.5 impaired the barrier function of eos-CRSwNP epithelial cells and increased the permeability of large molecules. PM2.5 also increased the secretion of pro-inflammatory cytokines by nasal epithelial cells. Budesonide could partially repair the damage, suggesting potential applications in clinical practice.

Project description:BackgroundCooks exposed to biomass fuel experience increased risk of respiratory disease and mortality. We sought to characterize lung function and environmental exposures of primary cooking women using two fuel-types in southeastern India, as well as to investigate the effect of particulate matter (PM) from kitchens on human airway epithelial (HAE) cells in vitro.MethodsWe assessed pre- and post-bronchodilator lung function on 25 primary female cooks using wood biomass or liquified petroleum gas (LPG), and quantified exposures from 34 kitchens (PM2.5, PM < 40 μm, black carbon, endotoxin, and PM metal and bacterial content). We then challenged HAE cells with PM, assessing its cytotoxicity to small-airway cells (A549) and its effect on: transepithelial conductance and macromolecule permeability (NuLi cells), and antimicrobial activity (using airway surface liquid, ASL, from primary HAE cells).ResultsLung function was impaired in cooks using both fuel-types. 60% of participants in both fuel-types had respiratory restriction (post bronchodilator FEV1/FVC>90). The remaining 40% in the LPG group had normal spirometry (post FEV1/FVC = 80-90), while only 10% of participants in the biomass group had normal spirometry, and the remaining biomass cooks (30%) had respiratory obstruction (post FEV1/FVC<80). Significant differences were found in environmental parameters, with biomass kitchens containing greater PM2.5, black carbon, zirconium, arsenic, iron, vanadium, and endotoxin concentrations. LPG kitchens tended to have more bacteria (p = 0.14), and LPG kitchen PM had greater sulphur concentrations (p = 0.02). In vitro, PM induced cytotoxicity in HAE A549 cells in a dose-dependent manner, however the effect was minimal and there were no differences between fuel-types. PM from homes of participants with a restrictive physiology increased electrical conductance of NuLi HAE cells (p = 0.06) and decreased macromolar permeability (p ≤ 0.05), while PM from homes of those with respiratory obstruction tended to increase electrical conductance (p = 0.20) and permeability (p = 0.07). PM from homes of participants with normal spirometry did not affect conductance or permeability. PM from all homes tended to inhibit antimicrobial activity of primary HAE cell airway surface liquid (p = 0.06).ConclusionsBiomass cooks had airway obstruction, and significantly greater concentrations of kitchen environmental contaminants than LPG kitchens. PM from homes of participants with respiratory restriction and obstruction altered airway cell barrier function, elucidating mechanisms potentially responsible for respiratory phenotypes observed in biomass cooks.

Dataset Information

Particulate Matter 2.5 Causes Deficiency in Barrier Integrity in Human Nasal Epithelial Cells.

Purpose

Methods

Results

Conclusions

Publications

Particulate Matter 2.5 Causes Deficiency in Barrier Integrity in Human Nasal Epithelial Cells.

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