ArticleFrontiers in microbiology2016
Pseudomonas aeruginosa Outer Membrane Vesicles Triggered by Human Mucosal Fluid and Lysozyme Can Prime Host Tissue Surfaces for Bacterial Adhesion.
Article in Frontiers in microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 63 citations in OpenAlex.
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- Bacterial Outer Membrane Vesicles: Research Advances from Biogenesis Mechanisms to Engineered Applications.Membranes · 2026Review
- Establishment and application of a vesicle extraction method for clinical strains ofMicrobiology spectrum · 2026Article
- Role of cell-associated and secretion-independent virulence factors of Pseudomonas aeruginosa in microbial keratitis and anti-virulence therapeutic strategies.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Review
- Outer membrane vesicles hijack TIM-1 for cellular uptake.PLoS pathogens · 2026Article
- Socio-evolutionary role of bacterial membrane vesicles in cooperation and competition within microbial communities.The ISME journal · 2026Review
- Prior contact lens wear reduces susceptibility of the superficially-injured cornea to bacterial adhesion.PloS one · 2026Article
- Deciphering the immunomodulatory cross-talk: Bacterial extracellular vesicles in gut homeostasis.Virulence · 2025Review
- Interplay Between Bacterial Extracellular Vesicles and Phages: Receptors, Mechanisms, and Implications.Viruses · 2025Review
- CombattingAntibiotics (Basel, Switzerland) · 2025Review
- ThemBio · 2025Article
- Outer membrane vesicles from Pseudomonas aeruginosa induce autophagy-regulated pyroptosis in THP-1 cells.Archives of microbiology · 2025Article
- Contact Lens Wear Alters Transcriptional Responses to Pseudomonas aeruginosa in Both the Corneal Epithelium and the Bacteria.Investigative ophthalmology & visual science · 2025Article
- Contact Lens Wear Alters Transcriptional Responses tobioRxiv : the preprint server for biology · 2024Article
- Extracellular vesicles released by host epithelial cells during Pseudomonas aeruginosa infection function as homing beacons for neutrophils.Cell communication and signaling : CCS · 2024Article
- Article
- Vesicular Messages from Dental Biofilms for Neutrophils.International journal of molecular sciences · 2024Article
- Cytotoxic rhamnolipid micelles drive acute virulence inInfection and immunity · 2024Article
- Cytotoxic rhamnolipid micelles drive acute virulence inbioRxiv : the preprint server for biology · 2023Article
- Pseudomonas aeruginosa-Derived Extracellular Vesicles Modulate Corneal Inflammation: Role in Microbial Keratitis?Infection and immunity · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Pseudomonas aeruginosa is a leading cause of human morbidity and mortality that often targets epithelial surfaces. Host immunocompromise, or the presence of indwelling medical devices, including contact lenses, can predispose to infection. While medical devices are known to accumulate bacterial biofilms, it is not well understood why resistant epithelial surfaces become susceptible to P. aeruginosa. Many bacteria, including P. aeruginosa, release outer membrane vesicles (OMVs) in response to stress that can fuse with host cells to alter their function. Here, we tested the hypothesis that mucosal fluid can trigger OMV release to compromise an epithelial barrier. This was tested using tear fluid and corneal epithelial cells in vitro and in vivo. After 1 h both human tear fluid, and the tear component lysozyme, greatly enhanced OMV release from P. aeruginosa strain PAO1 compared to phosphate buffered saline (PBS) controls (∼100-fold). Transmission electron microscopy (TEM) and SDS-PAGE showed tear fluid and lysozyme-induced OMVs were similar in size and protein composition, but differed from biofilm-harvested OMVs, the latter smaller with fewer proteins. Lysozyme-induced OMVs were cytotoxic to human corneal epithelial cells in vitro and murine corneal epithelium in vivo. OMV exposure in vivo enhanced Ly6G/C expression at the corneal surface, suggesting myeloid cell recruitment, and primed the cornea for bacterial adhesion (∼4-fold, P < 0.01). Sonication disrupted OMVs retained cytotoxic activity, but did not promote adhesion, suggesting the latter required OMV-mediated events beyond cell killing. These data suggest that mucosal fluid induced P. aeruginosa OMVs could contribute to loss of epithelial barrier function during medical device-related infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.