ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016
Pseudomonas aeruginosa exoenzymes U and Y induce a transmissible endothelial proteinopathy.
Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 37 citations in OpenAlex.
- PPM1B utilizes a trinuclear metal architecture for phosphatase activity.bioRxiv : the preprint server for biology · 2026Article
- Interplay between T3SS effectors, ExoY activation, and cGMP signaling in Pseudomonas aeruginosa infection.Nature communications · 2025Article
- cUMP elicits interendothelial gap formation duringAmerican journal of physiology. Lung cellular and molecular physiology · 2024Article
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- Oh my gut! Is the microbial origin of neurodegenerative diseases real?Infection and immunity · 2023Review
- Infection promotes Ser-214 phosphorylation important for generation of cytotoxic tau variants.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- New Insights into Clinical and Mechanistic Heterogeneity of the Acute Respiratory Distress Syndrome: Summary of the Aspen Lung Conference 2021.American journal of respiratory cell and molecular biology · 2022Article
- ExoU Induces Lung Endothelial Cell Damage and Activates Pro-Inflammatory Caspase-1 duringToxins · 2022Article
- Neurovascular Dysfunction in Diverse Communities With Health Disparities-Contributions to Dementia and Alzheimer's Disease.Frontiers in neuroscience · 2022Review
- Type I interferon signaling in SARS-CoV-2 associated neurocognitive disorder (SAND): Mapping host-virus interactions to an etiopathogenesis.Frontiers in neurology · 2022Review
- Perspectives on theToxins · 2021Review
- Carbonic Anhydrase IX and Hypoxia Promote Rat Pulmonary Endothelial Cell Survival during Infection.American journal of respiratory cell and molecular biology · 2021Article
- An Organ System-Based Synopsis ofVirulence · 2021Review
- Pneumonia initiates a tauopathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Cystatin C regulates the cytotoxicity of infection-induced endothelial-derived β-amyloid.FEBS open bio · 2020Article
- α-Tocopherol Attenuates the Severity ofAmerican journal of respiratory cell and molecular biology · 2020Article
- Exoenzyme Y induces extracellular active caspase-7 accumulation independent from apoptosis: modulation of transmissible cytotoxicity.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Antibodies Inhibiting the Type III Secretion System of Gram-Negative Pathogenic Bacteria.Antibodies (Basel, Switzerland) · 2020Review
- Virulent Pseudomonas aeruginosa infection converts antimicrobial amyloids into cytotoxic prions.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Pneumonia-induced endothelial amyloids reduce dendritic spine density in brain neurons.Scientific reports · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
We tested the hypothesis that Pseudomonas aeruginosa type 3 secretion system effectors exoenzymes Y and U (ExoY and ExoU) induce release of a high-molecular-weight endothelial tau, causing transmissible cell injury characteristic of an infectious proteinopathy. Both the bacterial delivery of ExoY and ExoU and the conditional expression of an activity-attenuated ExoU induced time-dependent pulmonary microvascular endothelial cell gap formation that was paralleled by the loss of intracellular tau and the concomitant appearance of high-molecular-weight extracellular tau. Transfer of the high-molecular-weight tau in filtered supernatant to naïve endothelial cells resulted in intracellular accumulation of tau clusters, which was accompanied by cell injury, interendothelial gap formation, decreased endothelial network stability in Matrigel, and increased lung permeability. Tau oligomer monoclonal antibodies captured monomeric tau from filtered supernatant but did not retrieve higher-molecular-weight endothelial tau and did not rescue the injurious effects of tau. Enrichment and transfer of high-molecular-weight tau to naïve cells was sufficient to cause injury. Thus we provide the first evidence for a pathophysiological stimulus that induces release and transmissibility of high-molecular-weight endothelial tau characteristic of an endothelial proteinopathy.
Indexed as
Identifiers
What OpenQuestion holds
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.