Supplementing Glucose Intake Reverses the Inflammation Induced by a High-Fat Diet by Increasing the Expression of Siglec-E Ligands on Erythrocytes.

Supplementing Glucose Intake Reverses the Inflammation Induced by a High-Fat Diet by Increasing the Expression of Siglec-E Ligands on Erythrocytes.
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DOI:
10.1007/s10753-023-01932-0
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发表时间:
2024-03
期刊:
影响因子:
5.1
通讯作者:
Hongmei Liu;Jin Li;Niting Wu;Yuanting She;Yadan Luo;Yan Huang;Hongyu Quan;Wenying Fu
Hongmei Liu;Jin Li;Niting Wu;Yuanting She;Yadan Luo;Yan Huang;Hongyu Quan;Wenying Fu
中科院分区:
医学2区
文献类型:
--
作者:
Hongmei Liu;Jin Li;Niting Wu;Yuanting She;Yadan Luo;Yan Huang;Hongyu Quan;Wenying Fu

文献摘要

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Siglec-9/E是在免疫细胞上表达的细胞表面受体,并且可以被唾液酸聚糖配体激活以发挥免疫抑制作用。我们先前的研究表明,增加Siglec-9(小鼠Siglec-E的人类paramino-A)配体的表达可维持血流中功能性静止的免疫细胞,但Siglec-9配体改变对动脉粥样硬化形成的生物学效应尚未进一步研究。在本研究中,我们证明了动脉粥样硬化危险因素ox-LDL或高脂饮食可以降低红细胞上Siglec-9/E配体的表达。通过膳食补充葡萄糖(20%葡萄糖)引起的红细胞上Siglec-E配体表达增加具有抗炎作用,并且该机制与葡萄糖摄入相关。在高脂饮食喂养的apoE−/−小鼠中,补充葡萄糖可减少动脉粥样硬化病变和外周炎症的面积。这些数据表明,增加的全身性炎症通过增加红细胞上Siglec-9/E配体的表达而减弱。因此,Siglec-9/E配体可能是动脉粥样硬化治疗的有价值的靶点。
Siglec-9/E is a cell surface receptor expressed on immune cells and can be activated by sialoglycan ligands to play an immunosuppressive role. Our previous study showed that increasing the expression of Siglec-9 (the human paralog of mouse Siglec-E) ligands maintains functionally quiescent immune cells in the bloodstream, but the biological effects of Siglec-9 ligand alteration on atherogenesis were not further explored. In the present study, we demonstrated that the atherosclerosis risk factor ox-LDL or a high-fat diet could decrease the expression of Siglec-9/E ligands on erythrocytes. Increased expression of Siglec-E ligands on erythrocytes caused by dietary supplementation with glucose (20% glucose) had anti-inflammatory effects, and the mechanism was associated with glucose intake. In high-fat diet-fed apoE−/−mice, glucose supplementation decreased the area of atherosclerotic lesions and peripheral inflammation. These data suggested that increased systemic inflammation is attenuated by increasing the expression of Siglec-9/E ligands on erythrocytes. Therefore, Siglec-9/E ligands might be valuable targets for atherosclerosis therapy.