Russo Thomas A, McFadden Catherine D, Carlino-MacDonald Ulrike B, Beanan Janet M, Barnard Travis J, Johnson James R
Department of Medicine, University of Buffalo, New York 14214, USA.
Infect Immun. 2002 Dec;70(12):7156-60. doi: 10.1128/IAI.70.12.7156-7160.2002.
IroN was recently identified in the extracellular pathogenic Escherichia coli strain CP9. In this study experimental evidence demonstrating that IroN mediates utilization of the siderophore enterobactin was obtained, thereby establishing IroN as a catecholate siderophore receptor. In a mouse model of ascending urinary tract infection the presence of iroN contributed significantly to CP9's ability to colonize the mouse bladder, kidneys, and urine, evidence that IroN is a urovirulence factor. However, growth in human urine ex vivo and adherence to uroepithelial cells in vitro were equivalent for an isogenic mutant deficient in IroN (CP82) and its wild-type parent (CP9). Taken together, these findings establish that IroN is a siderophore receptor and a urovirulence factor. However, uncertainty exists as to the mechanism(s) via which IroN contributes to urovirulence.
铁(IroN)最近在细胞外致病性大肠杆菌菌株CP9中被发现。在本研究中,获得了实验证据,证明IroN介导铁载体肠杆菌素的利用,从而将IroN确立为儿茶酚铁载体受体。在上行性尿路感染的小鼠模型中,iroN的存在显著有助于CP9定殖于小鼠膀胱、肾脏和尿液的能力,这证明IroN是一种尿路致病因子。然而,在体外人尿液中生长以及在体外对尿上皮细胞的粘附方面,IroN缺陷的同基因突变体(CP82)与其野生型亲本(CP9)相当。综上所述,这些发现表明IroN是一种铁载体受体和尿路致病因子。然而,IroN促进尿路致病的机制尚不确定。