Diesel exhaust particles up-regulate interleukin-17A expression via ROS/NF-κB in airway epithelium

Chih Ming Weng, Meng Jung Lee, Jung Re He, Ming Wei Chao, Chun Hua Wang, Han Pin Kuo

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

IL-17A is implicated in many aspects of pathogenesis of severe asthma, including inducing neutrophilic inflammation, airway hyperresponsiveness, steroid insensitivity and airway remodeling. Diesel exhaust particles (DEP) emission from vehicles has been shown to expand Th17 cells to increase IL-17A release that contributes to DEP-mediated exacerbation of asthma severity. It is not known whether non-immune cells in airways may also release IL-17A in response to DEP exposure. In this study, We found IL-17A expression was upregulated in the epithelium of severe allergic asthma patients from high road traffic pollution areas compared to those in low. Furthermore, we found DEP concentration-dependently increased IL-17A synthesis and release by 122.3 ± 15.72% and 235.5 ± 18.37%, respectively in primary bronchial epithelial cells (PBEC), accompanied with increased ROS production. Pretreatment of ROS scavenger (NAC) significantly inhibited DEP-induced IL-17A mRNA expression. DEP-induced IκBα degradation can be inhibited by NAC. We also found DEP increased p65 and RelB subunits expression, and pretreatment of NF-κB inhibitor (SN50) also inhibited DEP-induced IL-17A expression. We further found DEP increased NF-κB subunit RelB recruitment to IL-17A promoter in PBEC and airway tissue of severe allergic asthma patients from high road traffic pollution areas. These results indicate DEP stimulates IL-17A expression in airway epithelium through ROS/NF-κB pathway, and provide a possible link between traffic pollution exposure and IL-17A-related responses in severe allergic asthma patients.

Original languageEnglish
Pages (from-to)1-8
Number of pages8
JournalBiochemical Pharmacology
Volume151
DOIs
Publication statusPublished - May 1 2018

Fingerprint

Vehicle Emissions
Interleukin-17
Up-Regulation
Epithelium
Asthma
Pollution
Epithelial Cells
Airway Remodeling
Th17 Cells
Steroids

Keywords

  • Diesel exhaust particles
  • Epithelial cell
  • IL-17A
  • NF-κB
  • Reactive oxygen species
  • Severe asthma

ASJC Scopus subject areas

  • Biochemistry
  • Pharmacology

Cite this

Diesel exhaust particles up-regulate interleukin-17A expression via ROS/NF-κB in airway epithelium. / Weng, Chih Ming; Lee, Meng Jung; He, Jung Re; Chao, Ming Wei; Wang, Chun Hua; Kuo, Han Pin.

In: Biochemical Pharmacology, Vol. 151, 01.05.2018, p. 1-8.

Research output: Contribution to journalArticle

Weng, Chih Ming ; Lee, Meng Jung ; He, Jung Re ; Chao, Ming Wei ; Wang, Chun Hua ; Kuo, Han Pin. / Diesel exhaust particles up-regulate interleukin-17A expression via ROS/NF-κB in airway epithelium. In: Biochemical Pharmacology. 2018 ; Vol. 151. pp. 1-8.
@article{c721c539fe6b42ca8ccd50c67cfcc425,
title = "Diesel exhaust particles up-regulate interleukin-17A expression via ROS/NF-κB in airway epithelium",
abstract = "IL-17A is implicated in many aspects of pathogenesis of severe asthma, including inducing neutrophilic inflammation, airway hyperresponsiveness, steroid insensitivity and airway remodeling. Diesel exhaust particles (DEP) emission from vehicles has been shown to expand Th17 cells to increase IL-17A release that contributes to DEP-mediated exacerbation of asthma severity. It is not known whether non-immune cells in airways may also release IL-17A in response to DEP exposure. In this study, We found IL-17A expression was upregulated in the epithelium of severe allergic asthma patients from high road traffic pollution areas compared to those in low. Furthermore, we found DEP concentration-dependently increased IL-17A synthesis and release by 122.3 ± 15.72{\%} and 235.5 ± 18.37{\%}, respectively in primary bronchial epithelial cells (PBEC), accompanied with increased ROS production. Pretreatment of ROS scavenger (NAC) significantly inhibited DEP-induced IL-17A mRNA expression. DEP-induced IκBα degradation can be inhibited by NAC. We also found DEP increased p65 and RelB subunits expression, and pretreatment of NF-κB inhibitor (SN50) also inhibited DEP-induced IL-17A expression. We further found DEP increased NF-κB subunit RelB recruitment to IL-17A promoter in PBEC and airway tissue of severe allergic asthma patients from high road traffic pollution areas. These results indicate DEP stimulates IL-17A expression in airway epithelium through ROS/NF-κB pathway, and provide a possible link between traffic pollution exposure and IL-17A-related responses in severe allergic asthma patients.",
keywords = "Diesel exhaust particles, Epithelial cell, IL-17A, NF-κB, Reactive oxygen species, Severe asthma",
author = "Weng, {Chih Ming} and Lee, {Meng Jung} and He, {Jung Re} and Chao, {Ming Wei} and Wang, {Chun Hua} and Kuo, {Han Pin}",
year = "2018",
month = "5",
day = "1",
doi = "10.1016/j.bcp.2018.02.028",
language = "English",
volume = "151",
pages = "1--8",
journal = "Biochemical Pharmacology",
issn = "0006-2952",
publisher = "Elsevier Inc.",

}

TY - JOUR

T1 - Diesel exhaust particles up-regulate interleukin-17A expression via ROS/NF-κB in airway epithelium

AU - Weng, Chih Ming

AU - Lee, Meng Jung

AU - He, Jung Re

AU - Chao, Ming Wei

AU - Wang, Chun Hua

AU - Kuo, Han Pin

PY - 2018/5/1

Y1 - 2018/5/1

N2 - IL-17A is implicated in many aspects of pathogenesis of severe asthma, including inducing neutrophilic inflammation, airway hyperresponsiveness, steroid insensitivity and airway remodeling. Diesel exhaust particles (DEP) emission from vehicles has been shown to expand Th17 cells to increase IL-17A release that contributes to DEP-mediated exacerbation of asthma severity. It is not known whether non-immune cells in airways may also release IL-17A in response to DEP exposure. In this study, We found IL-17A expression was upregulated in the epithelium of severe allergic asthma patients from high road traffic pollution areas compared to those in low. Furthermore, we found DEP concentration-dependently increased IL-17A synthesis and release by 122.3 ± 15.72% and 235.5 ± 18.37%, respectively in primary bronchial epithelial cells (PBEC), accompanied with increased ROS production. Pretreatment of ROS scavenger (NAC) significantly inhibited DEP-induced IL-17A mRNA expression. DEP-induced IκBα degradation can be inhibited by NAC. We also found DEP increased p65 and RelB subunits expression, and pretreatment of NF-κB inhibitor (SN50) also inhibited DEP-induced IL-17A expression. We further found DEP increased NF-κB subunit RelB recruitment to IL-17A promoter in PBEC and airway tissue of severe allergic asthma patients from high road traffic pollution areas. These results indicate DEP stimulates IL-17A expression in airway epithelium through ROS/NF-κB pathway, and provide a possible link between traffic pollution exposure and IL-17A-related responses in severe allergic asthma patients.

AB - IL-17A is implicated in many aspects of pathogenesis of severe asthma, including inducing neutrophilic inflammation, airway hyperresponsiveness, steroid insensitivity and airway remodeling. Diesel exhaust particles (DEP) emission from vehicles has been shown to expand Th17 cells to increase IL-17A release that contributes to DEP-mediated exacerbation of asthma severity. It is not known whether non-immune cells in airways may also release IL-17A in response to DEP exposure. In this study, We found IL-17A expression was upregulated in the epithelium of severe allergic asthma patients from high road traffic pollution areas compared to those in low. Furthermore, we found DEP concentration-dependently increased IL-17A synthesis and release by 122.3 ± 15.72% and 235.5 ± 18.37%, respectively in primary bronchial epithelial cells (PBEC), accompanied with increased ROS production. Pretreatment of ROS scavenger (NAC) significantly inhibited DEP-induced IL-17A mRNA expression. DEP-induced IκBα degradation can be inhibited by NAC. We also found DEP increased p65 and RelB subunits expression, and pretreatment of NF-κB inhibitor (SN50) also inhibited DEP-induced IL-17A expression. We further found DEP increased NF-κB subunit RelB recruitment to IL-17A promoter in PBEC and airway tissue of severe allergic asthma patients from high road traffic pollution areas. These results indicate DEP stimulates IL-17A expression in airway epithelium through ROS/NF-κB pathway, and provide a possible link between traffic pollution exposure and IL-17A-related responses in severe allergic asthma patients.

KW - Diesel exhaust particles

KW - Epithelial cell

KW - IL-17A

KW - NF-κB

KW - Reactive oxygen species

KW - Severe asthma

UR - http://www.scopus.com/inward/record.url?scp=85042764253&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85042764253&partnerID=8YFLogxK

U2 - 10.1016/j.bcp.2018.02.028

DO - 10.1016/j.bcp.2018.02.028

M3 - Article

VL - 151

SP - 1

EP - 8

JO - Biochemical Pharmacology

JF - Biochemical Pharmacology

SN - 0006-2952

ER -