Acute respiratory barrier disruption by ozone exposure in mice
File(s)
Author(s)
Type
Journal Article
Abstract
Ozone exposure causes irritation, airway hyperreactivity (AHR), inflammation of the airways, and destruction of alveoli (emphysema), the gas exchange area of the lung in human and mice. This review focuses on the acute disruption of the respiratory epithelial barrier in mice. A single high dose ozone exposure (1 ppm for 1 h) causes first a break of the bronchiolar epithelium within 2 h with leak of serum proteins in the broncho-alveolar space, disruption of epithelial tight junctions and cell death, which is followed at 6 h by ROS activation, AHR, myeloid cell recruitment, and remodeling. High ROS levels activate a novel PGAM5 phosphatase dependent cell-death pathway, called oxeiptosis. Bronchiolar cell wall damage and inflammation upon a single ozone exposure are reversible. However, chronic ozone exposure leads to progressive and irreversible loss of alveolar epithelial cells and alveoli with reduced gas exchange space known as emphysema. It is further associated with chronic inflammation and fibrosis of the lung, resembling other environmental pollutants and cigarette smoke in pathogenesis of asthma, and chronic obstructive pulmonary disease (COPD). Here, we review recent data on the mechanisms of ozone induced injury on the different cell types and pathways with a focus on the role of the IL-1 family cytokines and the related IL-33. The relation of chronic ozone exposure induced lung disease with asthma and COPD and the fact that ozone exacerbates asthma and COPD is emphasized.
Date Issued
2019-09-13
Date Acceptance
2019-08-28
Citation
Frontiers in Immunology, 2019, 10, pp.1-10
ISSN
1664-3224
Publisher
Frontiers Media
Start Page
1
End Page
10
Journal / Book Title
Frontiers in Immunology
Volume
10
Copyright Statement
© 2019 Sokolowska, Quesniaux, Akdis, Chung, Ryffel and Togbe. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY)(http://creativecommons.org/licenses/by/4.0/). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Identifier
http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000485333200001&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
Subjects
Science & Technology
Life Sciences & Biomedicine
Immunology
inflammation
cell death
interleukins
mucus
tight junctions
innate immunity
INDUCED AIRWAY INFLAMMATION
INDUCED LUNG INFLAMMATION
OXIDATIVE STRESS
PULMONARY-LESIONS
EPITHELIAL-CELLS
TYPE-2 IMMUNITY
CYTOKINE FAMILY
EXHALED BREATH
HYPERRESPONSIVENESS
IL-33
Publication Status
Published
Article Number
ARTN 2169
Date Publish Online
2019-09-13