内毒素-Toll样受体4（TLR4）通路诱导的炎症介质反应与湿热证之“热”、水通道蛋白（AQP）与湿热证之“湿”关系密切，AQP与内毒素亦存在被证实的联系，故湿热证病机可能在于肠道菌群移位释放的内毒素双线同步启动内毒素-TLR4通路和AQP的过表达，从而促发瀑布式级联反应，导致机体炎症介质反应及水液代谢紊乱，发展为湿热证证型。以湿重于热及热重于湿小鼠湿热证模型为核心，探索两种湿热证小鼠肠道菌群移位相关指标的差异、及“湿”“热”客观指标的差异，研究菌群移位、炎症因子、AQP三者的关系及其实质；并通过茵陈蒿、连翘及益生菌干预实验、AQP与炎症因子相关实验、无菌小鼠菌群移植实验，进一步验证性的研究菌群移位、炎症因子、AQP三者关系，力图证实肠道菌群移位触发炎症因子及AQP是湿热证的核心机制，为阐明其机理提供新途径、新靶点。

The relationship of inflammatory mediator reactions induced by endotoxin/Toll-like receptor4(TLR4) pathway with the heat of dampness-heat syndrome(DHS), and the relationship of aquaporin (AQP) with the dampness of DHS are both close. Meanwhile, the relationship between AQP and endotoxin was also proved..So pathogenesis of DHS may be that over-expressions of endotoxin-TLR4 pathway and AQP, which are started doubly-line and synchronously by endotoxin released by bacterial translocation(BT) from gut, accordingly inducing cascade reactions, leading to body inflammatory mediators reactions and metabolic disorders in water-humor, and then developing into DHS. .BT correlative index differences between two kinds of mouse models with DHS, and difference of “hot”and“cold” objective indexes were all detected to explore the relationship and its essence among BT, inflammatory factor and AQP, using mouse models with DHS with predominant dampness or heat respectively as the research cores. As well as, the intervene experiment of Artemisia capillaries, Fructus forsythia and probiotics, the relative experiment of AQP and inflammatory factor, and the translocation experiments of germ-free mousse were executed to verifiably explore the relationship among BT, inflammatory factor and AQP further, and by strive to prove that BT from gut inducing inflammatory factor and AQP is the core mechanism of DHS, to provide the new approaches and new target for explaining the mechanism.