我们预实验发现，无论是体外LPS刺激，还是在体肠缺血再灌注(I/R)损伤模型都能够促进巨噬细胞表面TLR4及EGFR受体的表达增加；抑制EGFR的磷酸化则能够显著抑制TLR4以及EGFR在巨噬细胞膜表达。进一步实验发现，LPS通过激活EGFR而激活Rab5a，激活以后的Rab5a能通过同时介导EGFR与TLR4的内吞而诱发后期大量的EGFR与TLR4受体从高尔基体运输到细胞膜上，增强炎症反应。但是有关1. Rab5a所介导的受体内吞是通过何种机制诱发后期的受体外送；2. 除了肠I/R损伤，EGFR抑制剂对于其它诱因（如体外循环）的内毒素血症是否也同样具有抑制炎症过度反应的作用；3. EGFR抑制剂治疗内毒血症的临床效果如何，目前还不清楚。这些问题的解决不仅能够拓展我们对内毒素血症以及多器官功能不全发病机制的基础认识，还能进一步推进EGFR抑制剂在急危重症器官保护中的应用。

In our pre-experiments, we found that both in vitro LPS treatment and in vivo intestinal ischemia-reperfusion (I/R)injury model can up-regulate the expression of TLR4 and EGFR receptors on the cell surface of macrophage. Inhibiting the phosphorylation of EGFR can significantly decrease the amount of TLR4 and EGFR on the surface of macrophage. Further study revealed LPS can activate Rab5a through EGFR and Rab5a mediated endocytosis at early stage is critical to promote a robust transportation of TLR4 and EGFR from inner cell to cell surface and subsequent enhanced cell response to LPS. However there are still several problems needing to be further addressed. First, what is the connection between the Rab5a mediated endocytosis and the exocytosis of TLR4 and EGFR. Second, besides intestinal ischemia-reperfusion(I/R)injury, whether EGFR inhibitor has the similar effect on the endotoxemia induced by other reasons, such as cardiopulmonary bypass. Third, how is the effect of EGFR inhibitor treatment on endotoxemic patients. To solve these problems, we can not only expand our basic understanding of the pathogenesis of endotoxemia and multiple organ dysfunction, but also promote the application of EGFR inhibitor in critical care and organ protection.