Airway hyperresponsiveness development and the toxicity of PM2.5

Airway hyperresponsiveness (AHR) is characterized by excessive bronchoconstriction in response to nonspecific stimuli, thereby leading to airway stenosis and increased airway resistance. AHR is recognized as a key characteristic of asthma and is associated with significant morbidity. At present, man...

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Published in:Environmental science and pollution research international Vol. 28; no. 6; pp. 6374 - 6391
Main Authors: Lu, Xi, Li, Rongqin, Yan, Xixin
Format: Journal Article
Language:English
Published: Berlin/Heidelberg Springer Berlin Heidelberg 01-02-2021
Springer Nature B.V
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Abstract Airway hyperresponsiveness (AHR) is characterized by excessive bronchoconstriction in response to nonspecific stimuli, thereby leading to airway stenosis and increased airway resistance. AHR is recognized as a key characteristic of asthma and is associated with significant morbidity. At present, many studies on the molecular mechanisms of AHR have mainly focused on the imbalance in Th1 / Th2 cell function and the abnormal contraction of airway smooth muscle cells. However, the specific mechanisms of AHR remain unclear and need to be systematically elaborated. In addition, the effect of air pollution on the respiratory system has become a worldwide concern. To date, numerous studies have indicated that certain concentrations of fine particulate matter (PM2.5) can increase airway responsiveness and induce acute exacerbation of asthma. Of note, the concentration of PM2.5 does correlate with the degree of AHR. Numerous studies exploring the toxicity of PM2.5 have mainly focused on the inflammatory response, oxidative stress, genotoxicity, apoptosis, autophagy, and so on. However, there have been few reviews systematically elaborating the molecular mechanisms by which PM2.5 induces AHR. The present review separately sheds light on the underlying molecular mechanisms of AHR and PM2.5-induced AHR.
AbstractList Airway hyperresponsiveness (AHR) is characterized by excessive bronchoconstriction in response to nonspecific stimuli, thereby leading to airway stenosis and increased airway resistance. AHR is recognized as a key characteristic of asthma and is associated with significant morbidity. At present, many studies on the molecular mechanisms of AHR have mainly focused on the imbalance in Th1/Th2 cell function and the abnormal contraction of airway smooth muscle cells. However, the specific mechanisms of AHR remain unclear and need to be systematically elaborated. In addition, the effect of air pollution on the respiratory system has become a worldwide concern. To date, numerous studies have indicated that certain concentrations of fine particulate matter (PM2.5) can increase airway responsiveness and induce acute exacerbation of asthma. Of note, the concentration of PM2.5 does correlate with the degree of AHR. Numerous studies exploring the toxicity of PM2.5 have mainly focused on the inflammatory response, oxidative stress, genotoxicity, apoptosis, autophagy, and so on. However, there have been few reviews systematically elaborating the molecular mechanisms by which PM2.5 induces AHR. The present review separately sheds light on the underlying molecular mechanisms of AHR and PM2.5-induced AHR.
Airway hyperresponsiveness (AHR) is characterized by excessive bronchoconstriction in response to nonspecific stimuli, thereby leading to airway stenosis and increased airway resistance. AHR is recognized as a key characteristic of asthma and is associated with significant morbidity. At present, many studies on the molecular mechanisms of AHR have mainly focused on the imbalance in Th1 / Th2 cell function and the abnormal contraction of airway smooth muscle cells. However, the specific mechanisms of AHR remain unclear and need to be systematically elaborated. In addition, the effect of air pollution on the respiratory system has become a worldwide concern. To date, numerous studies have indicated that certain concentrations of fine particulate matter (PM2.5) can increase airway responsiveness and induce acute exacerbation of asthma. Of note, the concentration of PM2.5 does correlate with the degree of AHR. Numerous studies exploring the toxicity of PM2.5 have mainly focused on the inflammatory response, oxidative stress, genotoxicity, apoptosis, autophagy, and so on. However, there have been few reviews systematically elaborating the molecular mechanisms by which PM2.5 induces AHR. The present review separately sheds light on the underlying molecular mechanisms of AHR and PM2.5-induced AHR.
Author Yan, Xixin
Lu, Xi
Li, Rongqin
Author_xml – sequence: 1
  givenname: Xi
  surname: Lu
  fullname: Lu, Xi
  organization: Department of Respiratory and Critical Care Medicine, The Second Hospital of Hebei Medical University
– sequence: 2
  givenname: Rongqin
  surname: Li
  fullname: Li, Rongqin
  organization: Department of Central Laboratory, The Second Hospital of Hebei Medical University
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  givenname: Xixin
  orcidid: 0000-0003-4014-6226
  surname: Yan
  fullname: Yan, Xixin
  email: xi_xin_yan@126.com
  organization: Department of Respiratory and Critical Care Medicine, The Second Hospital of Hebei Medical University
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33394441$$D View this record in MEDLINE/PubMed
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ID FETCH-LOGICAL-c412t-a2e68ed1ba698156592ab91c6b02563f7784623d0a35f77304818da64e9de6303
IEDL.DBID AEJHL
ISSN 0944-1344
IngestDate Tue Nov 19 05:14:39 EST 2024
Fri Nov 22 00:33:06 EST 2024
Wed Oct 16 00:45:02 EDT 2024
Sat Dec 16 12:10:20 EST 2023
IsPeerReviewed true
IsScholarly true
Issue 6
Keywords Inflammatory responses
Oxidative stress
Cell cycle alteration
Epigenetic alterations
Immune system imbalances
Cytoplasmic calcium concentration Apoptosis
Fine particulate matter (PM2.5)
Autophagy
Airway hyperresponsiveness
Asthma
Language English
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c412t-a2e68ed1ba698156592ab91c6b02563f7784623d0a35f77304818da64e9de6303
ORCID 0000-0003-4014-6226
PMID 33394441
PQID 2481412156
PQPubID 54208
PageCount 18
ParticipantIDs proquest_journals_2481412156
crossref_primary_10_1007_s11356_020_12051_w
pubmed_primary_33394441
springer_journals_10_1007_s11356_020_12051_w
PublicationCentury 2000
PublicationDate 2021-02-01
PublicationDateYYYYMMDD 2021-02-01
PublicationDate_xml – month: 02
  year: 2021
  text: 2021-02-01
  day: 01
PublicationDecade 2020
PublicationPlace Berlin/Heidelberg
PublicationPlace_xml – name: Berlin/Heidelberg
– name: Germany
– name: Heidelberg
PublicationTitle Environmental science and pollution research international
PublicationTitleAbbrev Environ Sci Pollut Res
PublicationTitleAlternate Environ Sci Pollut Res Int
PublicationYear 2021
Publisher Springer Berlin Heidelberg
Springer Nature B.V
Publisher_xml – name: Springer Berlin Heidelberg
– name: Springer Nature B.V
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Snippet Airway hyperresponsiveness (AHR) is characterized by excessive bronchoconstriction in response to nonspecific stimuli, thereby leading to airway stenosis and...
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springer
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SubjectTerms Air pollution
Air Pollution - adverse effects
Air pollution effects
Apoptosis
Aquatic Pollution
Asthma
Atmospheric Protection/Air Quality Control/Air Pollution
Autophagy
Bronchoconstriction
Contraction
Earth and Environmental Science
Ecotoxicology
Environment
Environmental Chemistry
Environmental Health
Environmental science
Genotoxicity
Helper cells
Humans
Inflammation
Inflammatory response
Lung
Lymphocytes T
Molecular modelling
Morbidity
Muscle contraction
Muscles
Oxidative stress
Particulate emissions
Particulate matter
Particulate Matter - toxicity
Phagocytosis
Respiratory Hypersensitivity
Respiratory system
Respiratory tract
Review Article
Smooth muscle
Stenosis
Toxicity
Waste Water Technology
Water Management
Water Pollution Control
Title Airway hyperresponsiveness development and the toxicity of PM2.5
URI https://link.springer.com/article/10.1007/s11356-020-12051-w
https://www.ncbi.nlm.nih.gov/pubmed/33394441
https://www.proquest.com/docview/2481412156
Volume 28
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