scholarly journals Escherichia coli DraE Adhesin-Associated Bacterial Internalization by Epithelial Cells Is Promoted Independently by Decay-Accelerating Factor and Carcinoembryonic Antigen-Related Cell Adhesion Molecule Binding and Does Not Require the DraD Invasin

2008 ◽  
Vol 76 (9) ◽  
pp. 3869-3880 ◽  
Author(s):  
Natalia Korotkova ◽  
Yuliya Yarova-Yarovaya ◽  
Veronika Tchesnokova ◽  
Nina Yazvenko ◽  
Mike A. Carl ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Adhesion ◽  
Epithelial Cells ◽  
Carcinoembryonic Antigen ◽  
Host Cells ◽  
Decay Accelerating Factor ◽  
E Coli ◽  
Related Cell ◽  
Bladder Cells ◽  
Tract Infections

ABSTRACT The Dr family of Escherichia coli adhesins are virulence factors associated with diarrhea and urinary tract infections. Dr fimbriae are comprised of two subunits. DraE/AfaE represents the major structural, antigenic, and adhesive subunit, which recognizes decay-accelerating factor (DAF) and carcinoembryonic antigen (CEA)-related cell adhesion molecules (CEACAMs) CEA, CEACAM1, CEACAM3, and CEACAM6 as binding receptors. The DraD/AfaD subunit caps fimbriae and has been implicated in the entry of Dr-fimbriated E. coli into host cells. In this study, we demonstrate that DAF or CEACAM receptors independently promote DraE-mediated internalization of E. coli by CHO cell transfectants expressing these receptors. We also found that DraE-positive recombinant bacteria adhere to and are internalized by primary human bladder epithelial cells which express DAF and CEACAMs. DraE-mediated bacterial internalization by bladder cells was inhibited by agents which disrupt lipid rafts, microtubules, and phosphatidylinositol 3-kinase (PI3K) activity. Immunofluorescence confocal microscopic examination of epithelial cells detected considerable recruitment of caveolin, β1 integrin, phosphorylated ezrin, phosphorylated PI3K, and tubulin, but not F-actin, by cell-associated bacteria. Finally, we demonstrate that the DraD subunit, previously implicated as an “invasin,” is not required for β1 integrin recruitment or bacterial internalization.

scholarly journals Establishment of a Persistent Escherichia coli Reservoir during the Acute Phase of a Bladder Infection

2001 ◽  
Vol 69 (7) ◽  
pp. 4572-4579 ◽  
Author(s):  
Matthew A. Mulvey ◽  
Joel D. Schilling ◽  
Scott J. Hultgren
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Epithelial Cells ◽  
Urinary Tract Infections ◽  
Bacterial Attachment ◽  
Bacterial Invasion ◽  
E Coli ◽  
Bladder Cells ◽  
Tract Infections

ABSTRACT The vast majority of urinary tract infections are caused by strains of uropathogenic Escherichia coli that encode filamentous adhesive organelles called type 1 pili. These structures mediate both bacterial attachment to and invasion of bladder epithelial cells. However, the mechanism by which type 1 pilus-mediated bacterial invasion contributes to the pathogenesis of a urinary tract infection is unknown. Here we show that type 1-piliated uropathogens can invade the superficial epithelial cells that line the lumenal surface of the bladder and subsequently replicate, forming massive foci of intracellular E. coli termed bacterial factories. In response to infection, superficial bladder cells exfoliate and are removed with the flow of urine. To avoid clearance by exfoliation, intracellular uropathogens can reemerge and eventually establish a persistent, quiescent bacterial reservoir within the bladder mucosa that may serve as a source for recurrent acute infections. These observations suggest that urinary tract infections are more chronic and invasive than generally assumed.

scholarly journals Dynamin2- and endothelial nitric oxide synthase–regulated invasion of bladder epithelial cells by uropathogenic Escherichia coli

2011 ◽  
Vol 192 (1) ◽  
pp. 101-110 ◽  
Author(s):  
Zhimin Wang ◽  
Ceba Humphrey ◽  
Nicole Frilot ◽  
Gaofeng Wang ◽  
Zhongzhen Nie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Escherichia Coli ◽  
Epithelial Cells ◽  
Uropathogenic Escherichia Coli ◽  
Host Cells ◽  
Bacterial Invasion ◽  
E Coli ◽  
Nos Inhibitors ◽  
Tract Infections ◽  
Endothelial Nitric Oxide

Invasion of bladder epithelial cells by uropathogenic Escherichia coli (UPEC) contributes to antibiotic-resistant and recurrent urinary tract infections (UTIs), but this process is incompletely understood. In this paper, we provide evidence that the large guanosine triphosphatase dynamin2 and its partner, endothelial nitric oxide (NO) synthase (NOS [eNOS]), mediate bacterial entry. Overexpression of dynamin2 or treatment with the NO donor S-nitrosothiols increases, whereas targeted reduction of endogenous dynamin2 or eNOS expression with ribonucleic acid interference impairs, bacterial invasion. Exposure of mouse bladder to small molecule NOS inhibitors abrogates infection of the uroepithelium by E. coli, and, concordantly, bacteria more efficiently invade uroepithelia isolated from wild-type compared with eNOS−/− mice. E. coli internalization promotes rapid phosphorylation of host cell eNOS and NO generation, and dynamin2 S-nitrosylation, a posttranslational modification required for the bacterial entry, also increases during E. coli invasion. These findings suggest that UPEC escape urinary flushing and immune cell surveillance by means of eNOS-dependent dynamin2 S-nitrosylation and invasion of host cells to cause recurrent UTIs.

scholarly journals The Repeat-In-Toxin Family Member TosA Mediates Adherence of Uropathogenic Escherichia coli and Survival during Bacteremia

2011 ◽  
Vol 80 (2) ◽  
pp. 493-505 ◽  
Author(s):  
Patrick D. Vigil ◽  
Travis J. Wiles ◽  
Michael D. Engstrom ◽  
Lev Prasov ◽  
Matthew A. Mulvey ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Urinary Tract ◽  
Virulence Factors ◽  
Upper Urinary Tract ◽  
Host Cells ◽  
Content Type ◽  
E Coli ◽  
Wide Range ◽  
Novel Target ◽  
Tract Infections

ABSTRACTUropathogenicEscherichia coli(UPEC) is responsible for the majority of uncomplicated urinary tract infections (UTI) and represents the most common bacterial infection in adults. UPEC utilizes a wide range of virulence factors to colonize the host, including the novel repeat-in-toxin (RTX) protein TosA, which is specifically expressed in the host urinary tract and contributes significantly to the virulence and survival of UPEC.tosA, found in strains within the B2 phylogenetic subgroup ofE. coli, serves as a marker for strains that also contain a large number of well-characterized UPEC virulence factors. The presence oftosAin anE. coliisolate predicts successful colonization of the murine model of ascending UTI, regardless of the source of the isolate. Here, a detailed analysis of the function oftosArevealed that this gene is transcriptionally linked to genes encoding a conserved type 1 secretion system similar to other RTX family members. TosA localized to the cell surface and was found to mediate (i) adherence to host cells derived from the upper urinary tract and (ii) survival in disseminated infections and (iii) to enhance lethality during sepsis (as assessed in two different animal models of infection). An experimental vaccine, using purified TosA, protected vaccinated animals against urosepsis. From this work, it was concluded that TosA belongs to a novel group of RTX proteins that mediate adherence and host damage during UTI and urosepsis and could be a novel target for the development of therapeutics to treat ascending UTIs.

scholarly journals Fur Represses Adhesion to, Invasion of, and Intracellular Bacterial Community Formation within Bladder Epithelial Cells and Motility in Uropathogenic Escherichia coli

2016 ◽  
Vol 84 (11) ◽  
pp. 3220-3231 ◽  
Author(s):  
Kumiko Kurabayashi ◽  
Tomohiro Agata ◽  
Hirofumi Asano ◽  
Haruyoshi Tomita ◽  
Hidetada Hirakawa
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Antimicrobial Agents ◽  
Host Cells ◽  
Type I ◽  
Wild Type ◽  
Content Type ◽  
Type I Fimbriae ◽  
Tract Infections

Uropathogenic Escherichia coli (UPEC) is a major pathogen that causes urinary tract infections (UTIs). This bacterium adheres to and invades the host cells in the bladder, where it forms biofilm-like polymicrobial structures termed intracellular bacterial communities (IBCs) that protect UPEC from antimicrobial agents and the host immune systems. Using genetic screening, we found that deletion of the fur gene, which encodes an iron-binding transcriptional repressor for iron uptake systems, elevated the expression of type I fimbriae and motility when UPEC was grown under iron-rich conditions, and it led to an increased number of UPEC cells adhering to and internalized in bladder epithelial cells. Consequently, the IBC colonies that the fur mutant formed in host cells were denser and larger than those formed by the wild-type parent strain. Fur is inactivated under iron-restricted conditions. When iron was depleted from the bacterial cultures, wild-type UPEC adhesion, invasion, and motility increased, similar to the case with the fur mutant. The purified Fur protein bound to regions upstream of fimA and flhD , which encode type I fimbriae and an activator of flagellar expression that contributes to motility, respectively. These results suggest that Fur is a repressor of fimA and flhD and that its repression is abolished under iron-depleted conditions. Based on our in vitro experiments, we conclude that UPEC adhesion, invasion, IBC formation, and motility are suppressed by Fur under iron-rich conditions but derepressed under iron-restricted conditions, such as in patients with UTIs.

scholarly journals Dynamic localisation of DamX regulates bacterial filamentation and division during UPEC dispersal from host cells

2021 ◽  
Author(s):  
Bill Soderstrom ◽  
Daniel O. Daley ◽  
Iain G. Duggin
Keyword(s):  
Escherichia Coli ◽  
Cell Division ◽  
Stress Response ◽  
Epithelial Cells ◽  
Membrane Fusion ◽  
Host Cells ◽  
Division Rings ◽  
Bladder Cells ◽  
Rod Cell

Uropathogenic Escherichia coli (UPEC) cells can grow into highly filamentous forms during infection of bladder epithelial cells, but this process is poorly understood. Herein we found that some UPEC filaments released from infected bladder cells in vitro grew very rapidly and by more than 100 μm before initiating division, whereas others did not survive, suggesting that filamentation is a stress response that promotes dispersal. The DamX bifunctional division protein, which is essential for UPEC filamentation, was initially non-localized but then assembled at multiple division sites in the filaments prior to division. DamX rings maintained consistent thickness during constriction and remained at the septum until after membrane fusion was completed, like in rod cell division. Our findings suggest a mechanism involving regulated dissipation of DamX, leading to division arrest and filamentation, followed by its reassembly into division rings to promote UPEC dispersal and survival during infection.

scholarly journals Poloxamer 338 Affects Cell Adhesion and Biofilm Formation in Escherichia coli: Potential Applications in the Management of Catheter-Associated Urinary Tract Infections

Pathogens ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 885
Author(s):  
Mariarita Stirpe ◽  
Benedetta Brugnoli ◽  
Gianfranco Donelli ◽  
Iolanda Francolini ◽  
Claudia Vuotto
Keyword(s):  
Escherichia Coli ◽  
Cell Adhesion ◽  
Urinary Tract ◽  
Urinary Tract Infections ◽  
Biofilm Formation ◽  
Attenuated Total Reflection ◽  
Water Contact ◽  
E Coli ◽  
Static Conditions ◽  
Tract Infections

Poloxamers are nontoxic, amphiphilic copolymers used in different formulations. Due to its surfactant properties, Poloxamer 338 (P388) is herein proposed as a strategy to avoid biofilm formation often causing recalcitrant catheter-associated urinary tract infections (CAUTI). The aim is to evaluate the ability of P388 coatings to affect the adhesion of Ec5FSL and Ec9FSL Escherichia coli strains on silicone urinary catheters. Attenuated total reflection infrared spectroscopy, atomic force microscopy, and static water contact angle measurement were employed to characterize the P388-coated silicone catheter in terms of amount of P388 layered, coating thickness, homogeneity, and hydrophilicity. In static conditions, the antifouling power of P388 was defined by comparing the E. coli cells adherent on a hydrophilic P388-adsorbed catheter segment with those on an uncoated one. A P388-coated catheter, having a homogeneous coverage of 35 nm in thickness, reduced of 0.83 log10 and 0.51 log10 the biofilm of Ec5FSL and Ec9FSL, respectively. In dynamic conditions, the percentage of cell adhesion on P388-adsorbed silicone channels was investigated by a microfluidic system, simulating the in vivo conditions of catheterized patients. As a result, both E. coli isolates were undetected. The strong and stable antifouling property against E. coli biofilm lead us to consider P388 as a promising anti-biofilm agent for CAUTIs control.

scholarly journals Pectic Oligosaccharides from Cranberry Prevent Quiescence and Persistence in the Uropathogenic Escherichia coli CFT073

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jiadong Sun ◽  
Robert W. Deering ◽  
Zhiyuan Peng ◽  
Laila Najia ◽  
Christina Khoo ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Chemical Compounds ◽  
Uropathogenic Escherichia Coli ◽  
Cranberry Juice ◽  
Persister Cells ◽  
E Coli ◽  
Pectic Oligosaccharides ◽  
Bladder Cells ◽  
Strain Cft073 ◽  
Tract Infections

AbstractUrinary tract infections (UTIs) caused by Escherichia coli create a large burden on healthcare and frequently lead to recurrent infections. Part of the success of E. coli as an uropathogenic bacterium can be attributed to its ability to form quiescent intracellular reservoirs in bladder cells and its persistence after antibiotic treatment. Cranberry juice and related products have been used for the prevention of UTIs with varying degrees of success. In this study, a group of cranberry pectic oligosaccharides (cPOS) were found to both inhibit quiescence and reduce the population of persister cells formed by the uropathogenic strain, CFT073. This is the first report detailing constituents of cranberry with the ability to modulate these important physiological aspects of uropathogenic E. coli. Further studies investigating cranberry should be keen to include oligosaccharides as part of the ‘active’ cocktail of chemical compounds.

scholarly journals Infective endocarditis caused by Enterobacteriaceae: phenotypic and molecular characterization of Escherichia coli and Klebsiella pneumoniae in Rio de Janeiro, Brazil

2021 ◽  
Author(s):  
Nathália L. Andrade ◽  
Ana Carolina da Cruz Campos ◽  
Andrea Maria Cabral ◽  
Paula Hesselberg Damasco ◽  
Jerome Lo-Ten-Foe ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Infective Endocarditis ◽  
Epithelial Cells ◽  
Klebsiella Pneumoniae ◽  
Biofilm Formation ◽  
Genetic Characteristics ◽  
E Coli ◽  
Virulence Phenotype ◽  
Tract Infections ◽  
Urinary Isolates

AbstractThe etiological agent for infective endocarditis (IE), a life-threatening disease, is usually gram-positive bacteria. However, gram-negative bacteria can rarely cause IE and 4% of cases are associated with morbidity and mortality. This study aimed to characterize Escherichia coli and Klebsiella pneumoniae isolates from the blood of patients with IE. The characteristics of blood isolates were compared with those of urinary isolates from patients with urinary tract infections (UTIs). The results of this study revealed that K. pneumoniae isolates from patients with IE were phylogenetically related to those from patients with UTI. Additionally, the resistance phenotype, resistance gene, virulence gene, and plasmid profiles were similar between the blood and urinary isolates. The isolates belonging to the sequence types (STs) 76, 36, 101 (K. pneumoniae), and 69 (E. coli) are reported to be associated with drug resistance. The Enterobacteriaceae isolates from patients with IE did not produce extended-spectrum β-lactamase or carbapenemase. Additionally, this study investigated the virulence phenotype, biofilm formation ability, and the ability to adhere to the epithelial cells in vitro of the isolates. The isolates from patients with IE exhibited weaker biofilm formation ability than the urinary isolates. All isolates from patients with IE could adhere to the renal epithelial cells. However, three isolates from patients with UTIs could not adhere to the epithelial cells. The closely related K. pneumoniae isolates (648, KP1, KP2, KP3, and KP4) could not form biofilms or adhere to the epithelial cells. In summary, the molecular analysis revealed that the genetic characteristics of IE-causing K. pneumoniae and E. coli were similar to those of UTI-causing isolates. These isolates belonged to the STs that are considered treatable. Genetically similar isolates did not exhibit the same virulence phenotype. Thus, these non-hypervirulent clones must be monitored as they can cause complex infections in susceptible hosts.

Sign in / Sign up

Export Citation Format

Share Document