Allergy Asthma Immunol Res.  2020 Jan;12(1):56-71. 10.4168/aair.2020.12.1.56.

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

Affiliations
  • 1Department of Otolaryngology Head and Neck Surgery, Beijing TongRen Hospital, Capital Medical University, Beijing, China. dr.luozhang@139.com, wangcs830@126.com
  • 2Beijing Key Laboratory of Nasal Diseases, Beijing Institute of Otolaryngology, Beijing, China.
  • 3Swiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Davos, Switzerland.
  • 4Christine Kühne-Center for Allergy Research and Education, Davos, Switzerland.

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.

Keyword

Epithelial cells; particulate matters; nasal mucosa; rhinitis; asthma; cytokines

MeSH Terms

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
Budesonide
Claudin-1
Cytokines
Fluorescein
Fluorescein-5-isothiocyanate
Interleukin-8
Occludin
Particulate Matter
RNA, Messenger
Full Text Links
  • AAIR
Actions
Cited
CITED
export Copy
Close
Share
  • Twitter
  • Facebook
Similar articles
    DB Error: unknown error