ROLE OF BACTERIAL LECTINS IN KIDNEY DISEASES

膀胱炎是泌尿系统疾病中最常见的实体， 占美国所有办公室访问量的1%。 膀胱炎可能导致 肾盂肾炎，这是终末期肾脏的主要原因之一， 疾病 大肠杆菌是人类泌尿道最常见的致病菌 感染（UTI）。 细菌特性与临床形式的关系 感染导致发现P菌毛作为急性感染的毒力因子， 肾盂肾炎 P粘附介导E.大肠杆菌转化为Gal-Gal rich 肾脏组织中的受体。 抑制附着可以保护 肾脏感染。 尽管经过多次努力， 尚未描述膀胱炎和慢性（CHP）肾盂肾炎。 我们最近的研究表明，26%的膀胱炎相关E。 大肠埃希菌和35%的慢性肾盂肾炎相关性大肠埃希菌。大肠杆菌（未发表），但 无症状菌尿和急性肾盂肾炎仅占6% 携带着另一种粘附基因，叫做Dr血凝素。 博士 血凝素可以附着于UT中Dr受体，从而允许细菌 殖民化 抑制组织粘附相互作用可能会保护 UT反对Dr+ E的殖民化。大肠杆菌感染，预防UT。 此时的 Dr血凝素和Dr受体对病原性的贡献 膀胱炎和慢性肾盂肾炎还没有很好的记录。 这项研究将：（1）确定DR受体在细胞中的位置， 不同品系小鼠组织中DR受体的定量 （3）构建Dr阴性小鼠模型 临床E. coli菌株IH 11128;（4）测定相对 Dr阴性IH 11128和Dr阳性亲本菌株对 在上行性UTI的小鼠模型中定殖UT;（5）测定持续性 以及Dr阳性E.大肠杆菌，以开发 慢性肾盂肾炎模型;（6）进一步描述流行病学特征 和Dr+ E的性质。大肠杆菌进行基因型和表型分析。

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studies have demonstrated that 26% of cystitis-associated E. coli and 35% of chronic pyelonephritis-associated E. coli (unpublished) but only 6% of those from asymptomatic bacteriuria and acute pyelonephritis carry genes of another type of adhesion, called Dr hemagglutinin.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.