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3D quantitative imaging of unprocessed live tissue reveals epithelial defense against bacterial adhesion and subsequent traversal requires MyD88Role of defensins in corneal epithelial barrier function against Pseudomonas aeruginosa traversalPseudomonas aeruginosa induces membrane blebs in epithelial cells, which are utilized as a niche for intracellular replication and motilityThe ADP-ribosylation domain of Pseudomonas aeruginosa ExoS is required for membrane bleb niche formation and bacterial survival within epithelial cells.Cytotoxic clinical isolates of Pseudomonas aeruginosa identified during the Steroids for Corneal Ulcers Trial show elevated resistance to fluoroquinolones.The impact of inoculation parameters on the pathogenesis of contact lens-related infectious keratitis.MicroRNA-762 is upregulated in human corneal epithelial cells in response to tear fluid and Pseudomonas aeruginosa antigens and negatively regulates the expression of host defense genes encoding RNase7 and ST2.Surfactant protein D contributes to ocular defense against Pseudomonas aeruginosa in a murine model of dry eye disease.Pseudomonas aeruginosa utilizes the type III secreted toxin ExoS to avoid acidified compartments within epithelial cellsDynamics of flagellum- and pilus-mediated association of Pseudomonas aeruginosa with contact lens surfaces.Pseudomonas aeruginosa-induced bleb-niche formation in epithelial cells is independent of actinomyosin contraction and enhanced by loss of cystic fibrosis transmembrane-conductance regulator osmoregulatory function.The importance of the Pseudomonas aeruginosa type III secretion system in epithelium traversal depends upon conditions of host susceptibilityPathogenesis of contact lens-associated microbial keratitisAdenylate cyclase activity of Pseudomonas aeruginosa ExoY can mediate bleb-niche formation in epithelial cells and contributes to virulence.Modulation of epithelial immunity by mucosal fluid.Human tear fluid protects against Pseudomonas aeruginosa keratitis in a murine experimental model.Pseudomonas aeruginosa Survival at Posterior Contact Lens Surfaces after Daily Wear.Mucosal fluid glycoprotein DMBT1 suppresses twitching motility and virulence of the opportunistic pathogen Pseudomonas aeruginosa.Microbial keratitis: could contact lens material affect disease pathogenesis?Pseudomonas aeruginosa Outer Membrane Vesicles Triggered by Human Mucosal Fluid and Lysozyme Can Prime Host Tissue Surfaces for Bacterial Adhesion.Why does the healthy cornea resist Pseudomonas aeruginosa infection?Dynamics of Pseudomonas aeruginosa association with anionic hydrogel surfaces in the presence of aqueous divalent-cation salts.Role of the corneal epithelial basement membrane in ocular defense against Pseudomonas aeruginosa.Corneal surface glycosylation is modulated by IL-1R and Pseudomonas aeruginosa challenge but is insufficient for inhibiting bacterial binding.Mutation of the phospholipase catalytic domain of the Pseudomonas aeruginosa cytotoxin ExoU abolishes colonization promoting activity and reduces corneal disease severity.Possible involvement of the division cycle in dispersal of Escherichia coli from biofilms.Expression of surfactant protein D in human corneal epithelial cells is upregulated by Pseudomonas aeruginosa.Human Tear Fluid Reduces Culturability of Contact Lens-Associated Pseudomonas aeruginosa Biofilms but Induces Expression of the Virulence-Associated Type III Secretion System.Mutation of csk, encoding the C-terminal Src kinase, reduces Pseudomonas aeruginosa internalization by mammalian cells and enhances bacterial cytotoxicity.Clearance of Pseudomonas aeruginosa from a healthy ocular surface involves surfactant protein D and is compromised by bacterial elastase in a murine null-infection model.Contributions of MyD88-dependent receptors and CD11c-positive cells to corneal epithelial barrier function against Pseudomonas aeruginosa.Contribution of ExsA-regulated factors to corneal infection by cytotoxic and invasive Pseudomonas aeruginosa in a murine scarification model.Role of Pseudomonas aeruginosa ExsA in penetration through corneal epithelium in a novel in vivo model.The rfb locus from Pseudomonas aeruginosa strain PA103 promotes the expression of O antigen by both LPS-rough and LPS-smooth isolates from cystic fibrosis patients.Pseudomonas aeruginosa strains with lipopolysaccharide defects exhibit reduced intracellular viability after invasion of corneal epithelial cells.Actin cytoskeleton disruption by ExoY and its effects on Pseudomonas aeruginosa invasion.Exposure of human corneal epithelial cells to contact lenses in vitro suppresses the upregulation of human beta-defensin-2 in response to antigens of Pseudomonas aeruginosa.IL-1R and MyD88 Contribute to the Absence of a Bacterial Microbiome on the Healthy Murine Cornea.Quantification of Bacterial Twitching Motility in Dense Colonies Using Transmitted Light Microscopy and Computational Image Analysis.The Impact of ExoS on Pseudomonas aeruginosa Internalization by Epithelial Cells Is Independent of fleQ and Correlates with Bistability of Type Three Secretion System Gene Expression.
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P50
description
onderzoeker
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researcher ORCID ID = 0000-0002-6885-2053
@en
name
David J Evans
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David J Evans
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David J Evans
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David J Evans
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type
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David J Evans
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David J Evans
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David J Evans
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David J Evans
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prefLabel
David J Evans
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David J Evans
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David J Evans
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David J Evans
@nl
P106
P1153
12798687600
P21
P31
P496
0000-0002-6885-2053