목적: Monocytes play a crucial role in the pathophysiology of obstructive sleep apnea (OSA) and its associated complications. This study investigates the impact of OSA treatment on monocyte-mediated inflammation by analyzing changes in key pro-inflammatory cytokines, monocyte subset distribution (M1/M2), and lipopolysaccharide (LPS) responsiveness. 방법:Peripheral blood mononuclear cells (PBMCs) were isolated from OSA patients before and after treatment. TNF-α and IL-1β levels were quantified to assess systemic inflammation. Monocyte subset distribution was analyzed based on surface marker expression. LPS stimulation assays were performed to determine monocyte reactivity. The correlation between these immune parameters and OSA severity, particularly the apnea- hypopnea index (AHI) and oxygen desaturation index (ODI), was analyzed. 결과:Post-treatment, TNF-α and IL-1β levels were significantly reduced, indicating a decrease in systemic inflammation. Monocyte subset distribution exhibited notable changes, with a significant reduction in M2 proportions, particularly in patients with severe OSA. Interestingly, the degree of M2 reduction correlated more strongly with ODI than AHI, with patients showing greater ODI improvement demonstrating the most pronounced decrease in M2 monocytes. Additionally, monocyte responsiveness to LPS stimulation was attenuated following treatment, particularly in patients with severe baseline ODI. 결론:OSA treatment reduces systemic inflammation by decreasing pro- inflammatory cytokines, altering monocyte subset distributions, and attenuating LPS-induced monocyte activation. The findings suggest that ODI is a more relevant marker than AHI in assessing systemic immune dysregulation and treatment response. These results highlight the importance of oxygen desaturation in driving monocyte-mediated inflammation in OSA, warranting further investigation into its long- term implications.