反复发作和耐药菌株增多是尿路感染（UTI）防治面临的重点和难点，尿道致病性大肠杆菌（UPEC）侵袭膀胱上皮细胞（BECs）成为细胞内寄生菌是导致UTI反复发作的主要因素。研究显示，FimH是介导UPEC侵袭BECs的关键；FimH\整合素α3、β1\FAK介导的UPEC侵袭BECs是UPEC成为胞内菌的经典途径，本课题在前期研究证实治疗UTI的有效方剂尿感方具有抗UPEC侵袭BECs的作用，且能抑制大肠杆菌fim表达的基础上，提出“对FimH\整合素α3、β1\FAK介导的UPEC侵袭BECs途径的调节是尿感方抗UTI的作用机制之一”的假说。本研究采用体内外感染模型，运用多种现代技术，从宿主细胞和致病菌两个方面，研究尿感方抗UPEC侵袭BECs的作用特点和对FimH\整合素α3、β1\FAK介导的UPEC侵袭BECs途径主要环节的影响，剖析尿感方抗UPEC侵袭BECs的作用机制。

Recurrent and drug-resistant strains are the main challenges in preventing and curing urinary tract infection (UTI).Uropathogenic Escherichia Coli (UPEC) invading bladder epithelial cells (BECs) and becoming intracellular parasitic bacteria is the main factor leading to recurrent UTI. Studies have shown that FimH is key to the mediation of UPEC invading BECs, UPEC mutants that lack FimH are unable to effectively invade BECs. FimH/α3, β1integrins/FAK signaling pathway has been demonstrated, in the latest research, as the crucial signaling pathway mediating the UPEC invading BECs. Our previous study confirmed that Niaogan prescription has a certain effect on reducing the invasion of UPEC into BECs and suppressing the expression of UPEC virulence gene fim. Thus we hypothesize that Niaogan prescription protect BECs from UPEC invasion by regulating FimH/α3、β1 integrins/FAK signaling pathway. For clarifying the mechanism of Niaogan prescription in abrogation of UPEC invading BECs from the host cells and pathogens, we would observe the major components of FimH/α3、β1 integrins/FAK signaling pathway in vivo and in vitro, analyze the characteristics of Niaogan prescription in abrogation of UPEC invading BECs with multidiscipline approaches ,such as microbiology, cytology and molecular biology.