ROLE OF BACTERIAL LECTINS IN KIDNEY DISEASES

膀胱炎是最常见的尿路疾病，占 占美国所有办公室访问的1%。膀胱炎可能导致 肾盂肾炎是终末期肾病的主要原因之一 疾病。 大肠埃希氏菌是人类尿路最常见的病原体 感染(尿路感染)。细菌学特性与临床分型的关系 感染导致P菌毛被发现为急性呼吸道感染的毒力因子 肾盂肾炎。P-黏附介导大肠杆菌与富含半乳糖的黏附 肾组织中的受体。对依恋的抑制保护了 来自殖民者的肾脏。尽管做了几次努力，一个类似的协会 尚未被描述为膀胱炎和慢性(CHP)肾盂肾炎。 我们最近的研究表明，26%的膀胱炎相关性E. 大肠埃希菌和35%的慢性肾盂肾炎相关性大肠杆菌(未发表)，但 只有6%的人患有无症状菌尿和急性肾盂肾炎 携带另一种类型的粘连基因，称为DR血凝素。博士 血凝素可能附着在UT的DR受体上，从而使细菌 殖民主义。抑制组织黏附相互作用可能会保护 UT抗DR+大肠杆菌定植，预防UT。在这个时候， DR血凝素和DR受体在血友病致病中的作用 膀胱炎和慢性肾盂肾炎还没有很好的文献记载。 这项拟议的研究将：(1)确定DR受体在脑内的位置 来自不同品系小鼠的组织；(2)DR受体的定量 (3)构建DR阴性 临床菌株IH-11128的突变株；(4)亲缘关系的测定 DR阴性亲本菌株IH 11128和DR阳性亲本菌株的免疫原性 UT在上行性尿路感染小鼠模型中的定植；(5)测定持续性 DR阳性大肠埃希菌诱导的尿路感染及其发病机制 慢性肾盂肾炎模型；(6)进一步描述流行病学 并通过基因分型和表型分析对DR+大肠杆菌的特性进行了研究。

Cystitis is the most common entity of urinary tract diseases, accounting for 1% of all office visits in the USA. Cystitis may lead to pyelonephritis, which is one of the main causes of end stage kidney disease. Escherichia coli is the most common pathogen of human urinary tract infection (UTI). Association of bacterial properties and clinical form of infection led to the discovery of P fimbriae as a virulence factor in acute pyelonephritis. P adhesions mediate attachment of E. coli to Gal-Gal rich receptors in the kidney tissue. Inhibition of attachment protects the kidney from colonization. Despite several efforts, a similar association has not been described for cystitis and chronic (CHP) pyelonephritis. Our recent studies have demonstrated that 26% of cystitis-associated E. coli and 35% of chronic pyelonephritis-associated E. coli (unpublished) but only 6% of those from asymptomatic bacteriuria and acute pyelonephritis carry genes of another type of adhesion, called Dr hemagglutinin. Dr hemagglutinin may attach to Dr receptor in UT and thereby allow bacterial colonization. Inhibition of the tissue-adhesion interaction might protect UT against colonization by Dr+ E. coli and prevent UT. At this time the contribution of Dr hemagglutinin and Dr receptors to pathogenicity of cystitis and chronic pyelonephritis has not been well documented. The proposed research will: (1) determine the locations of Dr receptors in tissues from different mouse strains; (2) quantitate the Dr receptor content in tissues of selected mouse strains; (3) construct Dr negative mutant of the clinical E. coli strain IH 11128; (4) determine the relative capacity of the Dr negative IH 11128 and Dr positive parent strain to colonize UT in a mouse model of ascending UTI; (5) determine persistence and pathogenesis of UTI induced by Dr positive E. coli in order to develop a model of chronic pyelonephritis; (6) further characterize epidemiology and properties of Dr+ E. coli by genotypic and phenotypic analysis.