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Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

Published on: March 21, 2021

Pulmonary and systemic response to atmospheric pollution.

James C Hogg¹, Stephen van Eeden

¹The James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, The University of British Columbia, Vancouver, British Columbia, Canada. jhogg@mrl.ubc.ca

Respirology (Carlton, Vic.)

|April 9, 2009

Summary

Air pollution impairs lung defenses, triggering systemic inflammation. This response exacerbates chronic obstructive pulmonary disease (COPD) and contributes to cardiovascular events like heart attacks and strokes.

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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure

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Published on: August 25, 2017

Area of Science:

Environmental Health
Pulmonary Medicine
Cardiovascular Research

Background:

Inhaled toxic particles and gases impair lung innate defenses, increasing epithelial permeability, reducing mucociliary clearance, and depressing macrophage function.
Lung cells and macrophages release inflammatory mediators upon exposure to atmospheric particles, detectable in sputum, BAL fluid, and blood.

Purpose of the Study:

To review evidence linking inflammatory mediators from inhaled pollutants to local lung and systemic immune responses.
To explore the potential role of these responses in exacerbating chronic obstructive pulmonary disease (COPD) and contributing to cardiovascular events.

Main Methods:

Review of experimental evidence on the effects of atmospheric particle exposure on lung and systemic inflammation.
Analysis of the mechanisms linking inflammatory mediators to bone marrow release, acute phase protein production, and vascular endothelium activation.

Main Results:

Exposure to atmospheric particles induces local lung and systemic inflammation.
This inflammatory response promotes leukocyte and platelet release, acute phase protein production, and vascular endothelium activation, favoring atherosclerotic plaque formation and destabilization.
In elderly individuals with COPD, this response may precipitate acute exacerbations.

Conclusions:

Inhaled pollutants trigger a dual inflammatory response impacting both lung health and cardiovascular stability.
The findings suggest a mechanism linking air pollution to COPD exacerbations and acute coronary syndromes, including myocardial infarction and stroke.