Advanced glycation end products facilitate bacterial adherence in urinary tract
infection in diabetic mice.
Authors Ozer A, Altuntas CZ, Izgi K, Bicer F, Hultgren SJ, Liu G, Daneshgari F
Submitted By Firouz Daneshgari on 6/9/2015
Status Published
Journal Pathogens and disease
Year 2015
Date Published 7/1/2015
Volume : Pages 73 : Not Specified
PubMed Reference 25986378
Abstract Diabetic individuals have increased susceptibility to urinary tract infection
(UTI), a common, painful condition. During diabetes mellitus, non-enzymatic
reactions between reducing sugars and protein amine groups result in excessive
production of advanced glycation end products (AGEs) that accumulate in tissues.
Since bacteria adhere to cell surfaces by binding to carbohydrates, we
hypothesized that adherence of bacteria to the bladder in diabetics may be
enhanced by accumulation of AGEs on urothelial surface proteins. Using a murine
model of UTI, we observed increased adherence of type 1 fimbriated uropathogenic
Escherichia coli (UPEC) to the bladder in streptozotocin-induced diabetic female
mice compared with age-matched controls, along with increased concentrations of
two common AGEs in superficial urothelial cells from diabetic bladders. Several
lectins with different specificities exhibited increased binding to urothelial
homogenates from diabetic mice compared with controls, and two of those lectins
also bound to AGEs. Furthermore, mannose-binding type 1 fimbriae isolated from
UPEC bound to different AGEs, and UPEC adherence to the bladder in diabetic
mice, were inhibited by pretreatment of mice with the AGE inhibitor
pyridoxamine. These results strongly suggest a role for urothelial AGE
accumulation in increased bacterial adherence during UTI in diabetes.

Investigators with authorship
Firouz DaneshgariCase Western Reserve
Guiming LiuCase Western Reserve