COPD is one of the high-risk factors for lung cancer, but the underlying mechanism is still unclear. Here, we performed single-cell RNA sequencing analysis on three COPD tissues, and three COPD-based lung cancer tissue (LCCOPD), and enrolled the scRNA-seq data of normal lung tissues, COPD tissues, lung cancer tissues, and LCCOPD tissues from the public database. We found that most immune cell types were significantly enriched in COPD groups, and the LCCOPD showed a differential enrichment of T-regs and macrophage subtypes in comparison with COPD. FOXP3 mRNA expression was significantly increased in LCOPD-related T-regs and positively associated with CTLA-4 and PD-1 to form an immunosuppressive environment. Macrophages from different pathological environments show significant differences in cell composition, pseudo-time trajectories, and phenotypic dominance. COPD-related macrophages were dominated by M1-type with increased cell proliferation. LCCOPD-related macrophages, dominated by M2-type and tumor-associated macrophages, had progressively enhanced immune population chemotaxis along the trajectory. Based on the public data, we found the overlap of COPD accelerated infiltration of T-regs and M2 macrophages. Several metabolic and cytokine pathways were down-regulated in COPD tissues and up-regulated in LCCOPD groups, such as the SREBP pathway, IL2, IFN-γ, glycolysis, and glutamine metabolism. Our study provided an extensive description of lung cancer overlapping COPD and revealed the association between COPD status and the formation of an immunosuppressive environment, which elucidates the role of COPD, as a high-risk factor, in the development of lung cancer.
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