The in vitro Effects of Advanced Glycation End Products on Basophil Functions
The in vitro Effects of Advanced Glycation End Products on Basophil Functions
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DOI：
10.1159/000327298
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发表时间：
2011-01-01
影响因子：
2.8
通讯作者：
Ohta, Ken
中科院分区：
文献类型：
--
作者：
Han, Kaiyu;Suzukawa, Maho;Ohta, Ken
背景资料：嗜碱性粒细胞被认为在过敏反应的发病机制中起关键作用，但它们在与全身异常（如代谢紊乱）相关的炎症中的作用仍不清楚。晚期糖基化终产物（AGEs）是在高糖疾病条件下产生的潜在重要物质。在这项体外研究中，我们研究了人类嗜碱性粒细胞的生物学功能是否可以受到AGEs的影响。研究方法：我们分析了AGEs对人嗜碱性粒细胞的各种功能和标志物的影响，包括CD 11b表达、凋亡、脱粒和细胞因子产生。结果如下：流式细胞术分析表明，新鲜分离的嗜碱性粒细胞表面上的AGEs（AGEs）受体的水平非常低，但明显上调IL-3。高浓度糖化白蛋白可诱导嗜碱性粒细胞凋亡。尽管糖化白蛋白不能影响表面CD 11b表达水平或触发嗜碱性粒细胞脱粒或产生IL-4和IL-13，但其剂量依赖性地诱导IL-6和IL-8分泌。结论：AGEs似乎作用于人嗜碱性粒细胞，它们抑制细胞的寿命，但引起炎症细胞因子的分泌。通过这些生物学变化，嗜碱性粒细胞可能在与AGEs水平升高的代谢障碍相关的炎症性疾病中发挥一些作用。版权所有（C）2011 S. Karger AG，巴塞尔
Background: Basophils are thought to play pivotal roles in the pathogenesis of allergic reactions, but their roles in inflammation associated with systemic abnormalities such as metabolic disorders remain largely unknown. Advanced glycation end products (AGEs) are potentially important substances produced in high-glucose disease conditions. In this in vitro study, we investigated whether the biological functions of human basophils can be influenced by AGEs. Methods: We analyzed the effects of AGEs on various functions and markers of human basophils, including CD11b expression, apoptosis, degranulation, and cytokine production. Results: Flow cytometric analysis indicated that the level of the receptor for AGEs (RAGE) on the surface of freshly isolated basophils was very low but was clearly upregulated by IL-3. Apoptosis of basophils was induced by high concentrations of glycated albumin. Although glycated albumin failed to affect the level of surface CD11b expression or to trigger degranulation or production of IL-4 and IL-13 in basophils, it dose-dependently induced IL-6 and IL-8 secretion. Conclusions: AGEs seem to act on human basophils; they suppress the cells' longevity but elicit secretion of inflammatory cytokines. Through these biological changes, basophils might play some roles in inflammatory conditions associated with metabolic disorders presenting elevated levels of AGEs. Copyright (C) 2011 S. Karger AG, Basel