The role of the epithelial cell in <I>Escherichia coli</I> induced neutrophil migration into the urinary tract

ABSTRACT. The urinary tract is frequently the source of Escherichia coli bacteremia. Bacteria from the urinary tract must cross an epithelial layer to enter the bloodstream. Hepatocyte growth factor (HGF) alters the polarity of Madin-Darby canine kidney (MDCK) epithelial cells. The role of cell polarity in determining renal epithelial resistance to Escherichia coli invasion is not well known. A model of polarized and HGF-treated MDCK epithelial cells grown on filters was used to study the role of epithelial cell polarity during the interaction of nonvirulent (XL1-Blue) and uropathogenic (J96) strains of Escherichia coli with renal epithelium. Basolateral exposure of MDCK cells to J96, but not XL1-Blue, resulted in loss of transepithelial resistance (TER), which was due to epithelial cytotoxicity and not degradation of epithelial junctional proteins by bacterial proteases. Apical exposure to both J96 and XL1-Blue did not alter TER. Pretreatment of polarized MDCK cell monolayers with HGF renders the cells sensitive to loss of TER and cytotoxicity by apical exposure to J96. Analysis by confocal microscopy demonstrated that HGF treatment of MDCK cell monolayers also greatly enhances adherence of J96 to the apical surface of the cell monolayer. These data demonstrate that the basolateral surface of polarized epithelia is more susceptible to J96 cytotoxicity. The data also support the hypothesis that processes that alter epithelial cell polarity increase sensitivity of epithelia to bacterial injury and adherence from the apical compartment.

Download Full-text

Erratum to “The role of P fimbriae for Escherichia Coli establishment and mucosal inflammation in the human urinary tract” [Int. J. Antimicrob. Agents 19 (2002) 522–538]

International Journal of Antimicrobial Agents ◽

10.1016/s0924-8579(02)00327-8 ◽

2003 ◽

Vol 21 (6) ◽

pp. 604

Author(s):

Björn Wullt

Keyword(s):

Escherichia Coli ◽

Urinary Tract ◽

Mucosal Inflammation

Download Full-text

Uropathogenic Escherichia coli-Induced Inflammation Alters Mouse Urinary Bladder Contraction via an Interleukin-6-Activated Inducible Nitric Oxide Synthase-Related Pathway

Infection and Immunity ◽

10.1128/iai.00013-09 ◽

2009 ◽

Vol 77 (8) ◽

pp. 3312-3319 ◽

Cited By ~ 9

Author(s):

Te I. Weng ◽

Hsiao Yi Wu ◽

Pei Ying Lin ◽

Shing Hwa Liu

Keyword(s):

Nitric Oxide ◽

Escherichia Coli ◽

Urinary Tract Infection ◽

Urinary Tract ◽

Urinary Bladder ◽

Tract Infection ◽

Interleukin 6 ◽

Electrical Field Stimulation ◽

E Coli

ABSTRACT Escherichia coli is the most common cause of urinary tract infection. Elevated blood and urine interleukin-6 (IL-6) levels have been shown in inflammatory urinary tract diseases. The role of IL-6 in mediating the urodynamic dysfunction in response to E. coli-induced urinary tract infection has not yet been fully elucidated. In this study, we investigated the role of IL-6 in the nitric oxide (NO)-triggered alteration of contractile responses in the urinary bladder under an E. coli-induced inflammatory condition. The electrical field stimulation (EFS)-evoked contractions of the isolated detrusor strips, and immunoblotting for detecting protein expression in the bladders was measured short term (1 h) or long term (6 or 24 h) after intraperitoneal injection of E. coli endotoxin (lipopolysaccharide [LPS]) or intravesical instillation of human pyelonephritogenic E. coli-J96 (O4:K6) strain or LPS into mice. IL-6 and NO productions were increased in the urinary bladders of mice 1 to 24 h after LPS or E. coli-J96 treatment. Inducible NO synthase (iNOS) expression and protein kinase C (PKC) activation and EFS-evoked detrusor contractions were increased in the bladders at 6 h after LPS or E. coli-J96 treatment, which could be reversed by anti-IL-6 antibody and iNOS inhibitor aminoguanidine. At 1 h after LPS administration, bladder NO generation, endothelial NOS expression, and EFS-evoked detrusor contractions were effectively increased, whereas anti-IL-6 antibody could not reverse these LPS-induced responses. These results indicate that IL-6 may play an important role in the iNOS/NO-triggered PKC-activated contractile response in urinary bladder during E. coli or LPS-induced inflammation.

Download Full-text

Role of Capsular Colanic Acid in Adhesion of Uropathogenic Escherichia coli

Applied and Environmental Microbiology ◽

10.1128/aem.69.8.4474-4481.2003 ◽

2003 ◽

Vol 69 (8) ◽

pp. 4474-4481 ◽

Cited By ~ 76

Author(s):

Andrea Hanna ◽

Michael Berg ◽

Valerie Stout ◽

Anneta Razatos

Keyword(s):

Escherichia Coli ◽

Urinary Tract ◽

Bacterial Adhesion ◽

Specific Binding ◽

Binding Interactions ◽

Colanic Acid ◽

Mutant Strains ◽

Tract Infections ◽

Repulsive Forces

ABSTRACT Urinary tract infections are the most common urologic disease in the United States and one of the most common bacterial infections of any organ system. Biofilms persist in the urinary tract and on catheter surfaces because biofilm microorganisms are resistant to host defense mechanisms and antibiotic therapy. The first step in the establishment of biofilm infections is bacterial adhesion; preventing bacterial adhesion represents a promising method of controlling biofilms. Evidence suggests that capsular polysaccharides play a role in adhesion and pathogenicity. This study focuses on the role of physiochemical and specific binding interactions during adhesion of colanic acid exopolysaccharide mutant strains. Bacterial adhesion was evaluated for isogenic uropathogenic Escherichia coli strains that differed in colanic acid expression. The atomic force microscope (AFM) was used to directly measure the reversible physiochemical and specific binding interactions between bacterial strains and various substrates as bacteria initially approach the interface. AFM results indicate that electrostatic interactions were not solely responsible for the repulsive forces between the colanic acid mutant strains and hydrophilic substrates. Moreover, hydrophobic interactions were not found to play a significant role in adhesion of the colanic acid mutant strains. Adhesion was also evaluated by parallel-plate flow cell studies in comparison to AFM force measurements to demonstrate that prolonged incubation times alter bacterial adhesion. Results from this study demonstrate that the capsular polysaccharide colanic acid does not enhance bacterial adhesion but rather blocks the establishment of specific binding as well as time-dependent interactions between uropathogenic E. coli and inert substrates.

Download Full-text

Role of S- and common-type I-fimbriae of Escherichia coli in experimental upper and lower urinary tract infection

Microbial Pathogenesis ◽

10.1016/0882-4010(87)90023-4 ◽

1987 ◽

Vol 2 (3) ◽

pp. 223-226 ◽

Cited By ~ 15

Author(s):

Reinhard Marre ◽

Jörg Hacker

Keyword(s):

Escherichia Coli ◽

Urinary Tract Infection ◽

Urinary Tract ◽

Lower Urinary Tract ◽

Common Type ◽

Type I ◽

Lower Urinary Tract Infection ◽

Type I Fimbriae ◽

Lower Urinary

Download Full-text

An in vitro model of catheter-associated urinary tract infections to investigate the role of uncommon bacteria on the Escherichia coli microbial consortium

Biochemical Engineering Journal ◽

10.1016/j.bej.2016.11.013 ◽

2017 ◽

Vol 118 ◽

pp. 64-69 ◽

Cited By ~ 4

Author(s):

Andreia S. Azevedo ◽

Carina Almeida ◽

Luciana C. Gomes ◽

Carla Ferreira ◽

Filipe J. Mergulhão ◽

...

Keyword(s):

Escherichia Coli ◽

Urinary Tract ◽

Urinary Tract Infections ◽

In Vitro Model ◽

Microbial Consortium ◽

Vitro Model ◽

Tract Infections

Download Full-text

Survival of uropathogenic Escherichia coli in the murine urinary tract is dependent on OmpR

Microbiology ◽

10.1099/mic.0.026187-0 ◽

2009 ◽

Vol 155 (6) ◽

pp. 1832-1839 ◽

Cited By ~ 22

Author(s):

William R. Schwan

Keyword(s):

Escherichia Coli ◽

Urinary Tract ◽

Wild Type Strain ◽

Response Regulator ◽

Phosphorylation Site ◽

Regulatory System ◽

Growth Defect ◽

Wild Type ◽

Log Reduction

Uropathogenic Escherichia coli (UPEC) can grow in environments with significantly elevated osmolarities, such as murine and human urinary tracts. OmpR is the response regulator part of a two-component OmpR–EnvZ regulatory system that responds to osmotic stresses. To determine the role of OmpR in UPEC survival, a ΔompR mutant was created in the UPEC clinical isolate NU149. The ΔompR mutant had a growth defect compared with the wild-type strain under osmotic stress conditions; this defect was complemented by the full-length ompR gene on a plasmid, but not with a mutant OmpR with an alanine substitution for aspartic acid at the phosphorylation site at position 55. Furthermore, the ΔompR mutant displayed up to 2-log reduction in bacterial cell numbers in murine bladders and kidneys compared with wild-type bacteria after 5 days of infection. The ability of the bacteria to survive was restored to wild-type levels when the ΔompR mutant strain was complemented with wild-type ompR, but not when the alanine-substituted ompR gene was used. This study has fulfilled molecular Koch's postulates by showing the pivotal role OmpR plays in UPEC survival within the murine urinary tract.

Download Full-text