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Generation of a Chronic Obstructive Pulmonary Disease Model in Mice by Repeated Ozone Exposure
Published on: August 25, 2017
Inflammatory response in mouse lungs to haze episodes under different backgrounds of particulate matter exposure
Yuanhang Zhang1, Yuteng Zhang1, Kai Liu1
1School of Environment, Nanjing Normal University, Nanjing, China.
Abstract:
Particulate matter (PM) toxicity has mostly been investigated through in vitro exposure or tracheal infusion in animal models. However, given the complexity of ambient conditions, most animal studies do not mimic real-life PM exposure. In this work, we established a novel integrated exposure model to study the dynamic inflammatory response and defense strategies in ambient PM-exposed mice. Three groups of male C57BL/6 mice were kept in three chambers with pre-exposure to filtered air (FA), unfiltered air (UFA), or the air with a low PM concentration (PM2.5 ≤ 75 μg/m3) (LPM), respectively, for 37 days. Then all three groups of mice were exposed to haze challenge for 3 days, followed by exposure in filtered air for 7 days to allow recovery. Our results suggest that following a haze challenge, the defense strategies of mice of filtered air (FA) and low PM (LPM) groups comprised a form of "counterattack", whereas the response of the unfiltered air (UFA) group could be viewed as a "silence". While the latter strategy protected the lung tissues of mice from acute inflammatory damage, it also foreshadowed the development of chronic inflammatory diseases. These findings contribute to explaining previously documented PM-associated pathogenic mechanisms.
Insights
Mice exposed to unfiltered air during a haze challenge showed a "silence" defense, protecting lungs acutely but risking chronic inflammation. Filtered air and low particulate matter (PM) groups mounted a "counterattack" response.
Area of Science:
- Environmental Health
- Toxicology
- Immunology
Background:
- Particulate matter (PM) toxicity studies often lack real-world ambient condition complexity.
- Existing animal models for PM exposure do not fully mimic environmental scenarios.
Purpose of the Study:
- To establish a novel integrated exposure model for studying dynamic inflammatory responses to ambient PM.
- To investigate defense strategies in mice exposed to varying PM concentrations and subsequent haze challenges.
Main Methods:
- Developed an integrated exposure model using three groups of mice exposed to filtered air (FA), unfiltered air (UFA), or low PM (LPM) for 37 days.
- Subjected all groups to a 3-day haze challenge, followed by a 7-day recovery period in filtered air.
- Analyzed dynamic inflammatory responses and defense strategies in lung tissues.
Main Results:
- Mice in FA and LPM groups exhibited a "counterattack" inflammatory response post-haze challenge.
- Mice in the UFA group displayed a "silence" defense strategy, characterized by suppressed acute inflammation.
- The "silence" strategy in UFA mice protected against immediate inflammatory damage but indicated potential for chronic inflammatory disease development.
Conclusions:
- The study highlights distinct defense strategies against PM and haze exposure in mice.
- The findings provide insights into PM-associated pathogenic mechanisms, differentiating acute protective responses from long-term disease risks.
- The novel integrated exposure model offers a more realistic approach to studying ambient PM effects.

