High Spp1 Levels in Macrophages Link Environmental Pollution to Emphysema Development, Key Finding for COPD - Video

Chronic obstructive pulmonary disease (COPD) is an inflammatory disease characterized by airway obstruction and loss of alveolar surface, together resulting in progressive and irreversible airflow limitations and shortage of breath. Chronic bronchitis and emphysema are two major phenotypes of the disease. Cigarette smoke (CS) is a long-known cause of COPD, and it accounts for more than 70% of COPD cases, as reported by

WHO,1 but the contribution of indoor and outdoor air pollution is increasingly acknowledged.

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. Lianyong Han, the lead author of the study 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.

This study reveals a crucial mediator to environmental particle pollution-related chronic lung disease development and provides a potential preventive target.

Ref: Lianyong Han, Verena Haefner, Ali Önder Yildirim, Heiko Adler, Tobias Stoeger; Carbonaceous particle exposure triggered accumulation of Osteopontin/SPP1+ macrophages contributes to emphysema development: MedComm, Vol 6(2). https://doi.org/10.1002/mco2.70061