ArticleCell communication and signaling : CCS2023
Bacterial extracellular vesicles repress the vascular protective factor RNase1 in human lung endothelial cells.
Article in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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18 citing papers in PubMed, 22 citations in OpenAlex.
- Bacterial extracellular vesicles indirectly destabilize a human stem cell-derived blood-brain barrier on-chip through pro-inflammatory stimulation of immune cells.Lab on a chip · 2026Article
- Tumor exosomes impact functional hallmarks of cancer.Cancer metastasis reviews · 2026Review
- Antibiotics modulate Escherichia coli-derived bacterial extracellular vesicle production and their upregulation of ICAM-1 in human endothelial cells.Biology open · 2026Article
- Bacterial extracellular vesicles indirectly destabilize a human stem cell-derived blood-brain barrier on-chip through pro-inflammatory stimulation of immune cells.bioRxiv : the preprint server for biology · 2026Article
- Bacterial extracellular vesicles in the initiation, progression and treatment of atherosclerosis.Gut microbes · 2025Review
- Standardizing Bacterial Extracellular Vesicle Purification: A Call for Consensus.Journal of microbiology and biotechnology · 2025Review
- Bacterial Extracellular Vesicles: Emerging Regulators in the Gut-Organ Axis and Prospective Biomedical Applications.Current microbiology · 2025Review
- Serum proteomic profiling reveals potential predictive indicators for coronary artery calcification in stable ischemic heart disease.Journal of molecular histology · 2025Article
- On the road: extracellular vesicles in intercellular communication.Cell communication and signaling : CCS · 2025Article
- Outer membrane vesicles from Pseudomonas aeruginosa induce autophagy-regulated pyroptosis in THP-1 cells.Archives of microbiology · 2025Article
- The role of programmed cell death in organ dysfunction induced by opportunistic pathogens.Critical care (London, England) · 2025Review
- Klebsiella pneumoniae-derived extracellular vesicles impair endothelial function by inhibiting SIRT1.Cell communication and signaling : CCS · 2025Article
- Identification of a Novel Intracellular Function of the Secreted Ribonuclease RNASE1 in Inhibiting Gene Expression.Molecular and cellular biology · 2025Article
- Mechanisms of lung endothelial cell injury and survival in pulmonary arterial hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024Review
- Genomic structural variation contributes to evolved changes in gene expression in high-altitude Tibetan sheep.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The Role of Bacterial Extracellular Vesicles in the Immune Response to Pathogens, and Therapeutic Opportunities.International journal of molecular sciences · 2024Review
- State of the Art on the Role ofMicroorganisms · 2024Review
- Review
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSepsis is one of the leading causes of death worldwide and characterized by blood stream infections associated with a dysregulated host response and endothelial cell (EC) dysfunction. Ribonuclease 1 (RNase1) acts as a protective factor of vascular homeostasis and is known to be repressed by massive and persistent inflammation, associated to the development of vascular pathologies. Bacterial extracellular vesicles (bEVs) are released upon infection and may interact with ECs to mediate EC barrier dysfunction. Here, we investigated the impact of bEVs of sepsis-related pathogens on human EC RNase1 regulation.
methodsbEVs from sepsis-associated bacteria were isolated via ultrafiltration and size exclusion chromatography and used for stimulation of human lung microvascular ECs combined with and without signaling pathway inhibitor treatments.
resultsbEVs from Escherichia coli, Klebsiella pneumoniae and Salmonella enterica serovar Typhimurium significantly reduced RNase1 mRNA and protein expression and activated ECs, while TLR2-inducing bEVs from Streptococcus pneumoniae did not. These effects were mediated via LPS-dependent TLR4 signaling cascades as they could be blocked by Polymyxin B. Additionally, LPS-free ClearColi™ had no impact on RNase1. Further characterization of TLR4 downstream pathways involving NF-кB and p38, as well as JAK1/STAT1 signaling, revealed that RNase1 mRNA regulation is mediated via a p38-dependent mechanism.
conclusionBlood stream bEVs from gram-negative, sepsis-associated bacteria reduce the vascular protective factor RNase1, opening new avenues for therapeutical intervention of EC dysfunction via promotion of RNase1 integrity. Video Abstract.
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