Related Experiment Video
Updated: Jul 22, 2026
Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
CD36 regulates LPS-induced acute lung injury by promoting macrophages M1 polarization
Shishuo Sun1, Yizhou Yao2, Chao Huang1
1Cancer Institute, the First Clinical Medical College, Xuzhou Medical University, Xuzhou, Jiangsu, PR China; Center of Clinical Oncology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, PR China; Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy, Cancer Institute, Xuzhou Medical University, Xuzhou, Jiangsu, PR China.
Abstract:
M1 polarization of macrophages works as a promoter in pathogenesis of acute lung injury / acute respiratory distress syndrome (ALI/ARDS) by the secretion of pro-inflammatory cytokines and recruiting other inflammatory cells. Lipopolysaccharide (LPS), a critical component of the wall of gram-negative bacteria, can induce M1 polarization and ALI. Recently, cluster of differentiation 36 (CD36) has been reported to be associated with inflammatory responses. However, it has not yet been clarified whether CD36 in macrophages is involved in LPS-induced ALI. Herein, we demonstrated that in macrophages, LPS-induced ALI was regulated by CD36. Loss of CD36 attenuated LPS-induced ALI by reducing M1 polarization. Mechanistically, CD36 promoted macrophage M1 polarization by regulating CD14 associated with TLR4 during LPS stimulation. The findings of this study, clarified the mechanism of LPS-induced ALI through CD36 in macrophages, which provides a potential target for the prevention and treatment of ALI.
Insights
Cluster of differentiation 36 (CD36) on macrophages promotes acute lung injury (ALI) by driving M1 polarization. Blocking CD36 reduces inflammation and protects against LPS-induced ALI, offering a new therapeutic target.
Area of Science:
- Immunology
- Cell Biology
- Pathophysiology
Background:
- Macrophage M1 polarization drives acute lung injury (ALI) by releasing inflammatory cytokines.
- Lipopolysaccharide (LPS) from gram-negative bacteria induces M1 polarization and ALI.
- Cluster of differentiation 36 (CD36) is implicated in inflammatory responses, but its role in LPS-induced ALI is unclear.
Purpose of the Study:
- To investigate the role of CD36 in macrophages during LPS-induced ALI.
- To elucidate the mechanism by which CD36 influences M1 polarization in response to LPS.
Main Methods:
- Utilized macrophage models to study LPS-induced inflammation.
- Assessed the impact of CD36 expression on M1 polarization and ALI development.
- Investigated the molecular pathways involving CD36, CD14, and TLR4.
Main Results:
- LPS-induced ALI was regulated by CD36 in macrophages.
- Loss of CD36 attenuated LPS-induced ALI by reducing M1 polarization.
- CD36 promoted M1 polarization via regulation of CD14 associated with TLR4 during LPS stimulation.
Conclusions:
- CD36 plays a crucial role in mediating LPS-induced M1 polarization and ALI.
- Targeting CD36 in macrophages presents a potential therapeutic strategy for ALI prevention and treatment.
