Nuclear receptor corepressor 1 deficiency exacerbates asthma by modulating macrophage polarization

作者：Chenchen Hou, Lifeng Yan, Ke Sun, Tianyu Zhou, Yuxin Zou, Weining Xiong, Sheng‐Zhong Duan · 发表于：Cell Death Discovery · 年份：2023 · DOI：10.1038/s41420-023-01724-3 · 被引用次数：11 · 研究领域：Asthma and respiratory diseases、Immune Cell Function and Interaction、IL-33, ST2, and ILC Pathways

Macrophage polarization plays an important role in asthma. Nuclear receptor corepressor 1 (NCOR1) plays an important role in metabolic and cardiovascular diseases by regulating the function of macrophages. The aim of this research was to examine the role and mechanism of macrophage NCOR1 in the development of asthma. We used ovalbumin (OVA) to induce macrophage NCOR1-deficient mice for asthma formation. Our results revealed that macrophage NCOR1 deficiency markedly enhanced allergic airway inflammation. In addition, NCOR1 deficiency in macrophages was found to enhance M2 polarization. Mechanistic studies suggested that NCOR1 promoted macrophage polarization by interacting with PPARγ, contributing to the pathogenesis of asthma. In conclusion, macrophage NCOR1 deficiency promoted the regulation of M2 programming by enhancing PPARγ expression to exacerbate asthma. Macrophage NCOR1 might be a potential target for the treatment of asthma.