细菌脂蛋白（BLP）诱导LPS交叉耐受的分子机理研究
基本信息
结项摘要
诱导宿主的免疫炎症细胞耐受以降低过度炎症反应，从而防止脓毒症的发生，是近年来研究关注的焦点之一。但BLP诱导对LPS交叉耐受的分子机制目前尚不清楚。采用免疫共沉淀联合western-blotting技术观察诱导LPS耐受或BLP交叉耐受后TLR2/4-MyD88复合物形成状况，并通过荧光标记在活细胞内研究上述复合物形成与耐受性的关系，在此基础上探讨细胞骨架影响TLR2/TLR4募集MyD88的可能机制。通过研究验证本项目提出的假设：即诱导LPS耐受后，TLR4-MyD88复合物的形成减少，但TLR2-MyD88复合物形成不受影响；BLP诱导交叉耐受后，无论以大剂量BLP或LPS再次刺激，TLR2-MyD88和TLR4-MyD88复合物形成均减少。本项目从一个新的角度解释LPS诱导耐受和BLP 诱导交叉耐受的差异，为寻找和发现防治脓毒症休克的新药物和新方案提供实验依据。
项目摘要
项目成果
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数据更新时间：2023-05-31
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