Jump to main content
US EPA
United States Environmental Protection Agency
Search
Search
Main menu
Environmental Topics
Laws & Regulations
About EPA
Health & Environmental Research Online (HERO)
Contact Us
Print
Feedback
Export to File
Search:
This record has one attached file:
Add More Files
Attach File(s):
Display Name for File*:
Save
Citation
Tags
HERO ID
3120097
Reference Type
Journal Article
Title
Effect of transient receptor potential vanilloid-1 on cough hypersensitivity induced by particulate matter 2.5
Author(s)
Lv, H; Yue, J; Chen, Z; Chai, S; Cao, X; Zhan, J; Ji, Z; Zhang, H; Dong, R; Lai, K
Year
2016
Is Peer Reviewed?
1
Journal
Life Sciences
ISSN:
0024-3205
EISSN:
1879-0631
Volume
151
Page Numbers
157-166
Language
English
PMID
26926080
DOI
10.1016/j.lfs.2016.02.064
Web of Science Id
WOS:000375728400020
Abstract
AIMS:
The mechanism of cough hypersensitivity induced by particulate matter 2.5 (PM2.5) still remains elusive. The current study was designed to explore the effect of transient receptor potential vanilloid-1 (TRPV1) on cough hypersensitivity in airway and central nervous system.
MAIN METHODS:
The PM2.5-induced chronic cough model of guinea pig was established by exposure to different doses of PM2.5 for three weeks. After exposure, the animals were microinjected with TRPV1 agonist, antagonist in the dorsal vagal complex respectively. Cough sensitivity was measured by determining the provocative concentration of citric acid inducing 5 or more coughs (C5). Airway inflammation was detected by hematoxylin eosin (HE) staining and Evans blue fluorescence, and substance P (SP) and TRPV1 expressions in airway were observed by immunohistochemical staining. TRPV1 expressions in the dorsal vagal complex were observed by immunofluorescence. Retrograde tracing by pseudorabies virus-Bartha (PRV-Bartha) was conducted to confirm the regulatory pathway between airway and central nervous system.
KEY FINDINGS:
PM2.5 induced TRPV1 expressions in both of airway and dorsal vagal complex and airway neurogenic inflammation. Microinjecting agonist and antagonist of TRPV1 into the dorsal vagal complex could induce SP expressions increase and decrease respectively which indicated that TRPV1 in the dorsal vagal complex could promote airway neurogenic inflammation and regulate the cough reflex sensitivity through neural pathways of vagal complex-airways.
SIGNIFICANCE:
These findings implicated the therapeutic potential of specific inhibition of TRPV1 in airway and central nervous system for chronic cough induced by PM2.5.
Keywords
PM2.5; Cough reflex sensitivity; TRPV1; SP; Neurogenic inflammation; Dorsal vagal complex
Tags
NAAQS
•
ISA-PM (2019)
Considered
In Scope
Mode of action
Home
Learn about HERO
Using HERO
Search HERO
Projects in HERO
Risk Assessment
Transparency & Integrity