Increasing S1P promotes M1 macrophage in chronic obstructive pulmonary disease and chronic obstructive pulmonary disease-obstructive sleep apnea overlap syndrome via S1PR1/HDAC1 signaling.

Background: Chronic obstructive pulmonary disease (COPD) is characterized by irreversible airflow limitation and chronic airway inflammation. Obstructive sleep apnea (OSA) is a common clinical condition with partial or complete pharyngeal collapses occurring repeatedly during sleep. COPD-OSA is the coexistence of COPD and OSA. Abnormal macrophages play important roles in COPD progression. Sphingosine-1-phosphate (S1P) has emerged as an important molecule in COPD. This study aimed to explore the change and potential functional mechanism of S1P in COPD and COPD-OSA. Methods: Flow cytometry (FCM) was used to detect the M1 and M2 macrophage cell ratio. Enzyme-linked immunosorbent assay (ELISA) was used to detect the S1P levels. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot were used to detect the expression levels of S1P receptor 1 (S1PR1) and histone deacetylase 1 (HDAC1). Cytokine levels were detected by multiple microsphere flow immunofluorescence assay. The THP-1 cells of Results: Firstly, we found that the ratio of pro-inflammatory M1 macrophage was increased in COPD and COPD-OSA patients [ Conclusions: This study suggested that increasing S1P levels could facilitate macrophage polarization toward M1 subtype in COPD and COPD-OSA, via enhancing S1PR1 signaling or inhibiting HDAC1 signaling.