Uropathogenic<i>Escherichia coli</i>Express Type 1 Fimbriae Only in Surface Adherent Populations Under Physiological Growth Conditions

Stærk, Kristian; Khandige, Surabhi; Kolmos, Hans Jørn; Møller‐Jensen, Jakob; Andersen, Thomas Emil

doi:10.1093/infdis/jiv422

Cited by 46 publications

(56 citation statements)

References 51 publications

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“…1D). Bacterial adhesion to bladder cells has been previously demonstrated to depend highly on type 1 pilus expression and the adhesin FimH (12,(43)(44)(45), which was observed in our experiments as well (SI Appendix, Fig. S1).…”

Section: Evaluation Of Upec Adhesion To Bladder Cells Through Traditisupporting

confidence: 81%

Phosphoethanolamine cellulose enhances curli-mediated adhesion of uropathogenic Escherichia coli to bladder epithelial cells

Hollenbeck

Antonoplis

Chai

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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Uropathogenic (UPEC) are the major causative agents of urinary tract infections, employing numerous molecular strategies to contribute to adhesion, colonization, and persistence in the bladder niche. Identifying strategies to prevent adhesion and colonization is a promising approach to inhibit bacterial pathogenesis and to help preserve the efficacy of available antibiotics. This approach requires an improved understanding of the molecular determinants of adhesion to the bladder urothelium. We designed experiments using a custom-built live cell monolayer rheometer (LCMR) to quantitatively measure individual and combined contributions of bacterial cell surface structures [type 1 pili, curli, and phosphoethanolamine (pEtN) cellulose] to bladder cell adhesion. Using the UPEC strain UTI89, isogenic mutants, and controlled conditions for the differential production of cell surface structures, we discovered that curli can promote stronger adhesive interactions with bladder cells than type 1 pili. Moreover, the coproduction of curli and pEtN cellulose enhanced adhesion. The LCMR enables the evaluation of adhesion under high-shear conditions to reveal this role for pEtN cellulose which escaped detection using conventional tissue culture adhesion assays. Together with complementary biochemical experiments, the results support a model wherein cellulose serves a mortar-like function to promote curli association with and around the bacterial cell surface, resulting in increased bacterial adhesion strength at the bladder cell surface.

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Section: Evaluation Of Upec Adhesion To Bladder Cells Through Traditisupporting

confidence: 81%

Phosphoethanolamine cellulose enhances curli-mediated adhesion of uropathogenic Escherichia coli to bladder epithelial cells

Hollenbeck

Antonoplis

Chai

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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“…Moreover, the composition of human urine has a noticeable influence on the virulence of UPEC 10 11 . Generally, chemical exchange primarily accounts for metabolic interaction of UPEC and human urine and can be characterized as the “interactive metabolome”, which includes the utilized metabolome (metabolic cost) and excreted metabolome (metabolic donation) triggered by the interaction between UPEC and cultured human urine, by which the strains are capable of maintaining pathogenic growth in women’s bladders as the fundamental driver for causing infection 45 46 47 48 49 . In this study, we employed a combination of metabolomics and genetics 4 5 6 to discover and characterize the individualized interactive metabolome between UPEC and human urine that should be significantly differentiated from that between non-UPEC and human urine when the defined strains are cultured in pooled human urine.…”

Section: Discussionmentioning

confidence: 99%

Siderophore biosynthesis coordinately modulated the virulence-associated interactive metabolome of uropathogenic Escherichia coli and human urine

Guan

2016

Sci Rep

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Uropathogenic Escherichia coli (UPEC) growth in women’s bladders during urinary tract infection (UTI) incurs substantial chemical exchange, termed the “interactive metabolome”, which primarily accounts for the metabolic costs (utilized metabolome) and metabolic donations (excreted metabolome) between UPEC and human urine. Here, we attempted to identify the individualized interactive metabolome between UPEC and human urine. We were able to distinguish UPEC from non-UPEC by employing a combination of metabolomics and genetics. Our results revealed that the interactive metabolome between UPEC and human urine was markedly different from that between non-UPEC and human urine, and that UPEC triggered much stronger perturbations in the interactive metabolome in human urine. Furthermore, siderophore biosynthesis coordinately modulated the individualized interactive metabolome, which we found to be a critical component of UPEC virulence. The individualized virulence-associated interactive metabolome contained 31 different metabolites and 17 central metabolic pathways that were annotated to host these different metabolites, including energetic metabolism, amino acid metabolism, and gut microbe metabolism. Changes in the activities of these pathways mechanistically pinpointed the virulent capability of siderophore biosynthesis. Together, our findings provide novel insights into UPEC virulence, and we propose that siderophores are potential targets for further discovery of drugs to treat UPEC-induced UTI.

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“…Bayer silicones, Germany) in custom‐built flow chambers (method described previously in (Andersen et al, ; Stærk, Khandige, Kolmos, Møller‐Jensen, & Andersen, )) using the same seeding steps and growth conditions as outlined for the catheter biofilm model. Plasma was here supplemented with fluorescent human fibrinogen.…”

Section: Methodsmentioning

confidence: 99%

A novel in vitro model for haematogenous spreading ofS. aureusdevice biofilms demonstrating clumping dispersal as an advantageous dissemination mechanism

Grønnemose

Sæderup

Kolmos

et al. 2017

Cellular Microbiology

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Staphylococcus aureus is able to disseminate from vascular device biofilms to the blood and organs, resulting in life-threatening infections such as endocarditis. The mechanisms behind spreading are largely unknown, especially how the bacterium escapes immune effectors and antibiotics in the process. Using an in vitro catheter infection model, we studied S. aureus biofilm growth, late-stage dispersal, and reattachment to downstream endothelial cell layers. The ability of the released biofilm material to resist host response and disseminate in vivo was furthermore studied in whole blood and phagocyte survival assays and in a short-term murine infection model. We found that S. aureus biofilms formed in flow of human plasma release biofilm thromboemboli with embedded bacteria and bacteria-secreted polysaccharides. The emboli disseminate as antibiotic and immune resistant vehicles that hold the ability to adhere to and initiate colonisation of endothelial cell layers under flow. In vivo experiments showed that the released biofilm material reached the heart similarly as ordinary broth-grown bacteria but also that clumps to some extend were trapped in the lungs. The clumping dispersal of S. aureus from in vivo-like vascular biofilms and their specific properties demonstrated here help explain the pathophysiology associated with S. aureus bloodstream infections.

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UropathogenicEscherichia coliExpress Type 1 Fimbriae Only in Surface Adherent Populations Under Physiological Growth Conditions

Cited by 46 publications

References 51 publications

Phosphoethanolamine cellulose enhances curli-mediated adhesion of uropathogenic Escherichia coli to bladder epithelial cells

Phosphoethanolamine cellulose enhances curli-mediated adhesion of uropathogenic Escherichia coli to bladder epithelial cells

Siderophore biosynthesis coordinately modulated the virulence-associated interactive metabolome of uropathogenic Escherichia coli and human urine

A novel in vitro model for haematogenous spreading ofS. aureusdevice biofilms demonstrating clumping dispersal as an advantageous dissemination mechanism

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