The major metabolic feature of diabetes is hyperglycemia which has been linked to the diabetes inflammatory processes, and diabetes-related vulnerability to infection. In the present study, we assessed how glucose affected PBMCs in type I interferon (IFN) production and subsequent signaling. We found that the moderately elevated glucose promoted, and high glucose suppressed type I IFN production, respectively. Pre-exposure to high glucose rendered monocytes more sensitive to IFN-α stimulation with heightened signaling, whereas, instantaneous addition of high glucose did not exhibit such effect. Consistent with this finding, the mRNA levels of IFN-α-induced IRF-7 in PBMCs were positively correlated with HbA1c levels of diabetes patients. Additionally, we found that high glucose promoted the production of other proinflammatory cytokines/chemokines. This study suggests that hyperglycemia may affect the inflammatory process in diabetes via promoting proinflammatory cytokines, as well as the host defense against microbial infections through impeding type I IFN production and signaling.

中文翻译：

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高葡萄糖对人外周血免疫细胞产生细胞因子的影响以及单核细胞中I型干扰素的信号传导：高血糖在糖尿病炎症过程中的作用以及宿主抵抗感染的作用。

糖尿病的主要代谢特征是高血糖症，它与糖尿病的炎症过程以及与糖尿病相关的感染易感性有关。在本研究中，我们评估了葡萄糖如何影响I型干扰素（IFN）产生和后续信号传导中的PBMC。我们发现适度升高的葡萄糖分别促进了，而高葡萄糖抑制了I型IFN的产生。预先暴露于高葡萄糖会使单核细胞对IFN-α刺激更敏感，并具有增强的信号传导能力，而瞬时添加高葡萄糖则不会表现出这种作用。与该发现一致的是，PBMC中IFN-α诱导的IRF-7的mRNA水平与糖尿病患者的HbA1c水平呈正相关。另外，我们发现高葡萄糖促进了其他促炎细胞因子/趋化因子的产生。