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Updated: Jul 12, 2026
Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
Published on: August 12, 2019
Reduction of monocyte activation and oxidative stress by phosphodiesterase 4 blockade in Behçet's syndrome
Yeling Liu1, Jingwen Wu1, Yiyuan Ao1
1Department of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College; National Clinical Research Center for Dermatologic and Immunologic Diseases, Ministry of Science & Technology, NO.1 Shuaifuyuan, Dongcheng District, Beijing, 100730, China.
Objectives:
Behçet's syndrome (BS) is a systemic vasculitis characterized by multisystemic inflammatory manifestations driven by innate and adaptive immunity. Apremilast, an oral small-molecule selective inhibitor of phosphodiesterase 4 (PDE4), has shown effectiveness in treating oral ulcers of BS in both randomized clinical trials and real-world studies. This study aimed to explore the potential molecular mechanisms of apremilast in BS.
Methods:
Bulk RNA sequencing of peripheral blood mononuclear cells (PBMCs) from 15 BS patients undergoing apremilast treatment was performed. We evaluated reactive oxygen species (ROS) production by flow cytometry, as well as pro-inflammatory cytokine secretion and the transcriptomic signatures of monocytes before and after apremilast.
Results:
Transcriptomic analysis revealed that apremilast treatment was associated with the suppression of oxidative stress and inflammatory pathways in PBMCs, along with a decrease in the proportion of monocytes. Integrative analysis identified BACH1 as a potential transcriptional regulator downregulated following treatment. In vitro, apremilast reduced ROS levels and proinflammatory cytokine expression in monocytes, effects that were partially recapitulated by BACH1 silencing.
Conclusion:
Apremilast is associated with the reduction of monocyte-driven inflammatory and oxidative stress signatures in BS, potentially involving the downregulation of BACH1. Key Points • Apremilast reduces inflammatory and oxidative stress signatures in the PBMCs of BS patients, primarily by targeting monocyte-driven inflammation. • The anti-inflammatory effects of apremilast in monocytes are potentially mediated through the downregulation of the transcription factor BACH1.
