Particulate Matter 2.5 Causes Deficiency in Barrier Integrity in Human Nasal Epithelial Cells
10.4168/aair.2020.12.1.56
- Author:
Mu XIAN
1
;
Siyuan MA
;
Kuiji WANG
;
Hongfei LOU
;
Yang WANG
;
Luo ZHANG
;
Chengshuo WANG
;
Cezmi A AKDIS
Author Information
1. Department of Otolaryngology Head and Neck Surgery, Beijing TongRen Hospital, Capital Medical University, Beijing, China. dr.luozhang@139.com, wangcs830@126.com
- Publication Type:Original Article
- Keywords:
Epithelial cells;
particulate matters;
nasal mucosa;
rhinitis;
asthma;
cytokines
- MeSH:
Asthma;
Budesonide;
Claudin-1;
Cytokines;
Enzyme-Linked Immunosorbent Assay;
Epithelial Cells;
Fluorescein;
Fluorescein-5-isothiocyanate;
Fluorescent Antibody Technique;
Humans;
Interleukin-8;
Mucous Membrane;
Nasal Mucosa;
Occludin;
Particulate Matter;
Permeability;
Polymerase Chain Reaction;
Rhinitis;
RNA, Messenger;
Tight Junctions
- From:Allergy, Asthma & Immunology Research
2020;12(1):56-71
- CountryRepublic of Korea
- Language:English
-
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 μm (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 µg/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 µg/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.
