Dynamin2- and endothelial nitric oxide synthase–regulated invasion of bladder epithelial cells by uropathogenic <i>Escherichia coli</i>

Wang, Zhimin; Humphrey, Ceba; Frilot, Nicole; Wang, Gaofeng; Nie, Zhongzhen; Moniri, Nader H.; Daaka, Yehia

doi:10.1083/jcb.201003027

Cited by 26 publications

(24 citation statements)

References 37 publications

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“…It has been reported before that some UPEC strains are able to invade host bladder cells and to reproduce inside the host cell forming IBCs and that T1P contribute directly to the process of internalization [5]–[8]. Thus, we assayed CFT073 Δ ecpA for invasion of HeLa and HTB-4 cells through the gentamycin-protection assay.…”

Section: Resultsmentioning

confidence: 99%

Production of the Escherichia coli Common Pilus by Uropathogenic E. coli Is Associated with Adherence to HeLa and HTB-4 Cells and Invasion of Mouse Bladder Urothelium

et al. 2014

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Uropathogenic Escherichia coli (UPEC) strains cause urinary tract infections and employ type 1 and P pili in colonization of the bladder and kidney, respectively. Most intestinal and extra-intestinal E. coli strains produce a pilus called E. coli common pilus (ECP) involved in cell adherence and biofilm formation. However, the contribution of ECP to the interaction of UPEC with uroepithelial cells remains to be elucidated. Here, we report that prototypic UPEC strains CFT073 and F11 mutated in the major pilin structural gene ecpA are significantly deficient in adherence to cultured HeLa (cervix) and HTB-4 (bladder) epithelial cells in vitro as compared to their parental strains. Complementation of the ecpA mutant restored adherence to wild-type levels. UPEC strains produce ECP upon growth in Luria-Bertani broth or DMEM tissue culture medium preferentially at 26°C, during incubation with cultured epithelial cells in vitro at 37°C, and upon colonization of mouse bladder urothelium ex vivo. ECP was demonstrated on and inside exfoliated bladder epithelial cells present in the urine of urinary tract infection patients. The ability of the CFT073 ecpA mutant to invade the mouse tissue was significantly reduced. The presence of ECP correlated with the architecture of the biofilms produced by UPEC strains on inert surfaces. These data suggest that ECP can potentially be produced in the bladder environment and contribute to the adhesive and invasive capabilities of UPEC during its interaction with the host bladder. We propose that along with other known adhesins, ECP plays a synergistic role in the multi-step infection of the urinary tract.

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Section: Resultsmentioning

confidence: 99%

Production of the Escherichia coli Common Pilus by Uropathogenic E. coli Is Associated with Adherence to HeLa and HTB-4 Cells and Invasion of Mouse Bladder Urothelium

et al. 2014

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“…One of the final steps of the internalization process leading to the formation of nascent, UPEC-containing Rab27b-positive vesicles within the host cytosol is catalyzed by the large GTPase dynamin2 (82, 92, 93). The activity of dynamin2 is enhanced by S-nitrosylation of a single cysteine residue via reaction with nitric oxide (NO) that is generated by endothelial NO synthase (NOS3) (92, 93).…”

Section: Mechanisms Of Bladder Cell Invasion By Upecmentioning

confidence: 99%

“…The activity of dynamin2 is enhanced by S-nitrosylation of a single cysteine residue via reaction with nitric oxide (NO) that is generated by endothelial NO synthase (NOS3) (92, 93). Within the bladder, the levels of NO and other reactive nitrogen species rapidly increase in response to infection (94).…”

Section: Mechanisms Of Bladder Cell Invasion By Upecmentioning

confidence: 99%

Invasion of Host Cells and Tissues by Uropathogenic Bacteria

2016

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Within the mammalian urinary tract uropathogenic bacteria face many challenges, including the shearing flow of urine, numerous antibacterial molecules, the bactericidal effects of phagocytes, and a scarcity of nutrients. These problems may be circumvented in part by the ability of uropathogenic Escherichia coli (UPEC) and several other uropathogens to invade the epithelial cells that line the urinary tract. By entering host cells, uropathogens can gain access to additional nutrients and protection from both host defenses and antibiotic treatments. Translocation through host cells can facilitate bacterial dissemination within the urinary tract, while the establishment of stable intracellular bacterial populations may create reservoirs for relapsing and chronic urinary tract infections (UTIs). Here we review the mechanisms and consequences of host cell invasion by uropathogenic bacteria, with consideration of the defenses that are brought to bear against facultative intracellular pathogens within the urinary tract. The relevance of host cell invasion to the pathogenesis of UTIs in human patients is also assessed, along with some of the emerging treatment options that build upon our growing understanding of the infectious life cycle of UPEC and other uropathogenic bacteria.

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“…Forced overexpression of dynamin1 C607A, for example, reduces rate of agonist-induced β2AR internalization [47]. Similarly, overexpression of dynamin2 C86/607A decreases the bacteria invasion of bladder epithelial cells [107]. Drp1 S-nitrosylation triggers mitochondrial fission, synaptic loss, and neuronal damage that are key mediators of Alzheimer’s disease [105].…”

Section: Dynamin S-nitrosylationmentioning

confidence: 99%

S-nitrosylation-regulated GPCR signaling

Daaka

2012

Biochimica et Biophysica Acta (BBA) - General Subjects

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G protein-coupled receptors (GPCRs) are the most numerous and diverse type of cell surface receptors, accounting for about 1% of the entire human genome and relaying signals from a variety of extracellular stimuli that range from lipid and peptide growth factors to ions and sensory inputs. Activated GPCRs regulate a multitude of target cell functions, including intermediary metabolism, growth and differentiation, and migration and invasion. The GPCRs contain a characteristic 7-transmembrane domain topology and their activation promotes complex formation with a variety of intracellular partner proteins, which form basis for initiation of distinct signaling networks as well as dictate fate of the receptor itself. Both termination of active GPCR signaling and removal from the plasma membrane are controlled by protein post-translational modifications of the receptor itself and its interacting partners. Phosphorylation, acylation and ubiquitination are the most studied post-translational modifications involved in GPCR signal transduction, subcellular trafficking and overall expression. Emerging evidence demonstrates that protein S-nitrosylation, the covalent attachment of a nitric oxide moiety to specified cysteine thiol groups, of GPCRs and/or their associated effectors also participates in the fine-tuning of receptor signaling and expression. This newly appreciated mode of GPCR system modification adds another set of controls to more precisely regulate the many cellular functions elicited by this large group of receptors.

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

Abstract: eNOS-mediated S-nitrosylation of dynamin2 promotes infection of epithelial cells by E. coli.

Cited by 26 publications

References 37 publications

Production of the Escherichia coli Common Pilus by Uropathogenic E. coli Is Associated with Adherence to HeLa and HTB-4 Cells and Invasion of Mouse Bladder Urothelium

Production of the Escherichia coli Common Pilus by Uropathogenic E. coli Is Associated with Adherence to HeLa and HTB-4 Cells and Invasion of Mouse Bladder Urothelium

Invasion of Host Cells and Tissues by Uropathogenic Bacteria

S-nitrosylation-regulated GPCR signaling

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