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Published on: July 6, 2019
Pulmonary flora-modified diesel particulate matter induced lung injury via cGAS signaling pathway
Meng Sun1, Tong Wang1, Yemian Zhou1
1Anhui Province Key Laboratory of Environmental Toxicology and Pollution Control Technology, Key Laboratory of High Magnetic Field and Ion Beam Physical Biology, CAS, High Magnetic Field Laboratory, Hefei Institutes of Physical Science, CAS, Hefei, Anhui 230031, PR China; University of Science and Technology of China, Hefei, Anhui 230026, PR China.
Abstract:
Diesel particulate matter (DPM) is a major component of Fine Particulate Matter (PM2.5), which has been recognized by the World Health Organization under the name "Class I Carcinogen". Lung microbial communities are present widely in the lung tissue of a variety of organisms and play a significant role in the development and progression of lung disease, while cGAS is a DNA receptor that senses the invasion of microbial pathogens and activates the innate immune response. However, the role of cGAS in pulmonary flora-mediated PM2.5-induced lung injury is still largely unknown. With constructed cGAS-/- C57BL/6J mice, we found that lung damage, inflammation, and genetic damage induced by DPM were significantly blocked. With antibiotic-treated C57BL/6J mice, we found that healthy lung microbes were able to attenuate DPM-induced lung damage, inflammation, and genetic damage. DPM modified the expression of the cGAS/STING signaling pathway through the lung flora. This study revealed that cGAS signaling pathway played an essential role in lung flora-mediated adverse effects of DPM, which provided new therapeutic targets for lung diseases.
Insights
Diesel particulate matter (DPM) lung injury is mediated by lung microbes and the cGAS signaling pathway. Blocking cGAS or altering lung flora significantly reduced DPM-induced lung damage, inflammation, and genetic damage.
Area of Science:
- Environmental Health
- Immunology
- Microbiology
Background:
- Diesel particulate matter (DPM), a component of PM2.5, is a known carcinogen.
- Lung microbial communities influence lung disease development.
- The cGAS DNA receptor triggers innate immune responses to pathogens.
Purpose of the Study:
- To investigate the role of the cGAS signaling pathway in lung flora-mediated PM2.5-induced lung injury.
- To explore potential therapeutic targets for DPM-induced lung diseases.
Main Methods:
- Utilized cGAS knockout (cGAS-/-) C57BL/6J mice to assess DPM effects.
- Employed antibiotic treatment in C57BL/6J mice to study the impact of lung microbiota.
- Analyzed DPM-induced lung damage, inflammation, and genetic damage.
Main Results:
- DPM-induced lung damage, inflammation, and genetic damage were significantly reduced in cGAS-/- mice.
- Healthy lung microbes attenuated DPM-induced lung injury in antibiotic-treated mice.
- DPM exposure altered cGAS/STING pathway expression via lung flora.
Conclusions:
- The cGAS signaling pathway is crucial in lung flora-mediated DPM adverse effects.
- Lung microbiota play a significant role in PM2.5-induced lung injury.
- Targeting the cGAS pathway offers potential therapeutic strategies for lung diseases.
