Hyperglycemia-induced alterations of gut microflora and therapeutic strategy in a critically ill model

在这项研究中，我们检查了持续高血糖是否会引起危重病模型中肠道屏障功能的改变。在内毒素血症模型中，短期高血糖增加肠粘膜通透性，而长期高血糖24 h导致肠系膜淋巴结中炎性细胞因子如IL-1β和IL-6以及肠道中T淋巴细胞亚群如辅助性T2和调节性T细胞的上调。本研究揭示了临床相关水平的持续高血糖对危重病患者肠道屏障功能和免疫系统的显著影响。

In this study, we examined if persistent hyperglycemia elicited alterations of gut barrier function in a critical ill model. Short-term hyperglycemia augmented gut mucosal permeability in an endotoxemic model, while long-term hyperglycemia for 24hr resulted in the up-regulation of inflammatory cytokines such as IL-1β and IL-6 in mesenteric lymph nodes, and of T lymphocyte subset such as helper T2 and regulatory T cells in gut. The present study shed light on the significant effects of clinically relevant level of persistent hyperglycemia on gut barrier function and immune system in critical ill.