Sichuan International Medical Exchange and Promotion Association
This study is led by Dr. Lianyong Han and Dr. Tobias Stoeger in Germany (Institute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Zentrum München, German Research Center for Environmental Health).
By analyzing multiple emphysema and COPD patient datasets, SPP1 is significantly upregulated in the lungs of patients, compared to healthy individuals. "These findings pointed out the clinical relevance of SPP1 induction during COPD development and has motivated us to understand their contributions in depth," Dr. Han says.
In an experimental COPD model, Dr. Han has identified a sub-population of macrophages in the lung expressing high level of Spp1, and long-term cigarette smoking exposure caused persistent induction of Spp1 up to 6 months in these macrophages (Spp1+ macrophages). This finding is supported by advanced high-throughput single-cell RNA sequencing technique.
Similar to cigarette smoking, soot-like carbonaceous particles also caused long-term induction of Spp1, as well as the release of Osteopontin (OPN), a protein encoded by Spp1. "Consistently, OPN is also localized in macrophages in the lung, as revealed by our immunohistochemical staining," Dr. Han says.
In a previous study from the same team, scientists found in a "second-hit model", repeated carbonaceous particle exposure of gammaherpesvirus-infected mice caused lung emphysema. A further analysis by the team found a correlation between Spp1 induction and emphysema, subsequently highlighting the contribution of SPP1 to the development of air pollution-related COPD.
"Over 90% of the global population is still living in areas where air pollution levels exceed WHO guidelines of 10 μg/m for PM2.5, this is further aggravated by occupational exposure," Dr. Stoeger says. Thus, the persistent particle challenges in the real-world pose long-term damage and injury to the lung, which finally contributes to the development of chronic lung diseases.
This study reveals a crucial mediator to environmental particle pollution-related chronic lung disease development and provides a potential preventive target.
See the article here:
Carbonaceous particle exposure triggered accumulation of Osteopontin/SPP1+ macrophages contributes to emphysema development