Extracellular polysaccharide from Bordetella species reduces high glucose-induced macrophage apoptosis via regulating interaction between caveolin-1 and TLR4
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Updated: Apr 1, 2026
Legionella pneumophila Outer Membrane Vesicles: Isolation and Analysis of Their Pro-inflammatory Potential on Macrophages
Published on: February 22, 2017
Min Li1, Fei Lin2, Yanliang Lin3
1Department of Cardiology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
Abstract:
Microphage apoptosis is a critical event in atherosclerotic lesions in patients with diabetes. In the present investigation, high glucose treatment inhibited Akt phosphorylation and activated caspase 3 in primary peritoneal macrophage, leading to cell apoptosis. Hypoxia prolonged macrophage survival in high glucose condition. Extracellular polysaccharide from Bordetella species (EPS) further decreased cell apoptosis in response to high glucose during hypoxia. Under high glucose and hypoxic condition, EPS treatment promoted caveolin-1 phosphorylation by recognizing TLR4. Caveolin-1 phosphorylation elevated membrane Glut1 level to accelerate glucose consumption, which should be the reason for protective effect of EPS on macrophage exposed to high glucose. Further investigation demonstrated that TLR4-dependent caveolin-1 phosphorylation induced by EPS promoted association of caveolin-1 with TLR4, which should be critical for activation of TLR4 signaling pathway.
Insights
Extracellular polysaccharide (EPS) from Bordetella species protects macrophages from high glucose-induced apoptosis during hypoxia. This involves TLR4-dependent caveolin-1 phosphorylation, enhancing glucose uptake and promoting macrophage survival in diabetic atherosclerosis.
Area of Science:
- Biomedical Science
- Cell Biology
- Immunology
Background:
- Macrophage apoptosis is a key factor in atherosclerotic lesions, particularly in diabetic patients.
- High glucose levels in diabetes promote macrophage apoptosis by inhibiting Akt phosphorylation and activating caspase 3.
Purpose of the Study:
- To investigate the protective effects of extracellular polysaccharide (EPS) from Bordetella species on macrophages under high glucose and hypoxic conditions.
- To elucidate the molecular mechanisms underlying EPS-mediated protection.
Main Methods:
- Primary peritoneal macrophages were treated with high glucose and subjected to hypoxia.
- The effects of EPS on cell apoptosis, Akt phosphorylation, caspase 3 activation, caveolin-1 phosphorylation, and Glut1 levels were assessed.
- Toll-like receptor 4 (TLR4) involvement was investigated.
Main Results:
- High glucose induced macrophage apoptosis, while hypoxia prolonged survival.
- EPS treatment significantly reduced apoptosis in high glucose and hypoxic conditions.
- EPS promoted TLR4-dependent caveolin-1 phosphorylation, increasing membrane Glut1 levels and glucose consumption.
- EPS facilitated the association of caveolin-1 with TLR4, activating the TLR4 signaling pathway.
Conclusions:
- Extracellular polysaccharide (EPS) from Bordetella species confers a protective effect on macrophages against high glucose-induced apoptosis under hypoxic conditions.
- The protective mechanism involves the TLR4-caveolin-1 signaling pathway, leading to enhanced glucose uptake and reduced apoptosis, offering a potential therapeutic strategy for diabetic atherosclerosis.
