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Background: Macrophages play a crucial role in inflammatory diseases, including chronic obstructive pulmonary disease (COPD). MIR155 host gene (MIR155HG), a novel long non-coding RNA (lncRNA), has been recognized as a regulator of macrophage polarization, we thus investigated its role in COPD. Methods: We used granulocyte-macrophage colony-stimulating factor (GM-CSF) to induce peripheral blood mononuclear cells (PBMCs)-derived macrophages obtained from COPD patients and normal controls. Quantitative real-time PCR (QRT-PCR) was used to detect the expressions of MIR155HG and M1/M2 macrophage markers. The quantification of M1 and M2 macrophages was analyzed by flow cytometry. Enzyme-linked immunosorbent assay (ELISA) was conducted for testing the concentration of inflammatory cytokines. Results: MIR155HG was highly expressed in GM-CSF-induced macrophages of COPD patients. Further investigation demonstrated that MIR155HG overexpression promoted GM-CSF-induced M1 macrophage polarization and the release of pro-inflammatory cytokines. However, the knockdown of MIR-155HG could inhibit the polarization of M1 macrophages and increase M2 macrophage polarization. Conclusion: LncRNA MIR155HG modulated GM-CSF-mediated M1/M2 macrophage polarization in COPD progression.