ArticleCell communication and signaling : CCS2024
Extracellular vesicles released by host epithelial cells during Pseudomonas aeruginosa infection function as homing beacons for neutrophils.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- The miR-183/96/182 Cluster Regulates Trigeminal Ganglion Sensory Neurons' Response toPathogens (Basel, Switzerland) · 2026Article
- The miR-183/96/182 Cluster Regulates Trigeminal Ganglion Sensory Neurons' Response tobioRxiv : the preprint server for biology · 2026Article
- The Therapeutic Potential of Exosomes in Ocular Surface Diseases.Biomolecules · 2026Review
- Exosomes in corneal diseases: advances in diagnosis and therapy.Frontiers in cell and developmental biology · 2026Review
- Exosomes in Corneal Homeostasis and Wound Healing.Current eye research · 2025Review
- Extracellular vesicles in pulmonary diseases: roles and therapeutic potential.BMC pulmonary medicine · 2025Review
- Exosomes in Ocular Health: Recent Insights into Pathology, Diagnostic Applications and Therapeutic Functions.Biomedicines · 2025Review
- Tug of war: innate immunity and herpes simplex keratitis.Frontiers in immunology · 2025Review
- Article
- Epithelial extracellular vesicles induce inflammation and neutrophil activation in theFrontiers in immunology · 2025Article
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Authors and funding
3 authors.
Funding
Abstract
backgroundPseudomonas aeruginosa (PA) is an opportunistic pathogen that can cause sight threatening infections in the eye and fatal infections in the cystic fibrosis airway. Extracellular vesicles (EVs) are released by host cells during infection and by the bacteria themselves; however, there are no studies on the composition and functional role of host-derived EVs during PA infection of the eye or lung. Here we investigated the composition and capacity of EVs released by PA infected epithelial cells to modulate innate immune responses in host cells.
methodsHuman telomerase immortalized corneal epithelial cells (hTCEpi) cells and human telomerase immortalized bronchial epithelial cells (HBECs) were treated with a standard invasive test strain of Pseudomonas aeruginosa, PAO1, for 6 h. Host derived EVs were isolated by qEV size exclusion chromatography. EV proteomic profiles during infection were compared using mass spectrometry and functional studies were carried out using hTCEpi cells, HBECs, differentiated neutrophil-like HL-60 cells, and primary human neutrophils isolated from peripheral blood.
resultsEVs released from PA infected corneal epithelial cells increased pro-inflammatory cytokine production in naïve corneal epithelial cells and induced neutrophil chemotaxis independent of cytokine production. The EVs released from PA infected bronchial epithelial cells were also chemotactic although they failed to induce cytokine secretion from naïve HBECs. At the proteomic level, EVs derived from PA infected corneal epithelial cells exhibited lower complexity compared to bronchial epithelial cells, with the latter having reduced protein expression compared to the non-infected control.
conclusionsThis is the first study to comprehensively profile EVs released by corneal and bronchial epithelial cells during Pseudomonas infection. Together, these findings show that EVs released by PA infected corneal and bronchial epithelial cells function as potent mediators of neutrophil migration, contributing to the exuberant neutrophil response that occurs during infection in these tissues.
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