ArticleJournal of immunology (Baltimore, Md. : 1950)2012
ExoS and ExoT ADP ribosyltransferase activities mediate Pseudomonas aeruginosa keratitis by promoting neutrophil apoptosis and bacterial survival.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 98 citations in OpenAlex.
- Article
- Integrating resistance biology, virulence networks, and precision therapeutics against multidrug-resistant Pseudomonas aeruginosa.Infection · 2026Review
- Individual contributions of exotoxins S and T on internalizedInfection and immunity · 2026Article
- Genomic and Phenotypic Insights into Carbapenem-ResistantMicroorganisms · 2026Article
- Bactericidal activity of mammalian histones is caused by large membrane pore formation.Cell reports · 2025Article
- Bacteria detect neutrophils via a system that responds to hypochlorous acid and flow.bioRxiv : the preprint server for biology · 2025Article
- ExoS effector in Pseudomonas aeruginosa Hyperactive Type III secretion system mutant promotes enhanced Plasma Membrane Rupture in Neutrophils.PLoS pathogens · 2025Article
- Intracellular replication ofmSphere · 2023Article
- NLRP3 selectively drives IL-1β secretion by Pseudomonas aeruginosa infected neutrophils and regulates corneal disease severity.Nature communications · 2023Article
- Intracellular replication of Pseudomonas aeruginosa in epithelial cells requires suppression of the caspase-4 inflammasome.bioRxiv : the preprint server for biology · 2023Article
- Comparative Evaluation ofVision (Basel, Switzerland) · 2023Article
- Genetic and Environmental Investigation of a Novel Phenylamino Acetamide Inhibitor of the Pseudomonas aeruginosa Type III Secretion System.Applied and environmental microbiology · 2023Article
- Review
- Elevated c-di-GMP Levels and Expression of the Type III Secretion System Promote Corneal Infection by Pseudomonas aeruginosa.Infection and immunity · 2022Article
- Condensins are essential for Pseudomonas aeruginosa corneal virulence through their control of lifestyle and virulence programs.Molecular microbiology · 2022Article
- Exotoxin S secreted by internalized Pseudomonas aeruginosa delays lytic host cell death.PLoS pathogens · 2022Article
- Review
- Modulation of the immune response by theFrontiers in cellular and infection microbiology · 2022Review
- An Organ System-Based Synopsis ofVirulence · 2021Review
- Foundational concepts in the biology of bacterial keratitis.Experimental eye research · 2021Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pseudomonas aeruginosa is a leading cause of blinding corneal ulcers worldwide. To determine the role of type III secretion in the pathogenesis of P. aeruginosa keratitis, corneas of C57BL/6 mice were infected with P. aeruginosa strain PAO1 or PAK, which expresses ExoS, ExoT, and ExoY, but not ExoU. PAO1- and PAK-infected corneas developed severe disease with pronounced opacification and rapid bacterial growth. In contrast, corneas infected with ΔpscD or ΔpscJ mutants that cannot assemble a type III secretion system, or with mutants lacking the translocator proteins, do not develop clinical disease, and bacteria are rapidly killed by infiltrating neutrophils. Furthermore, survival of PAO1 and PAK strains in the cornea and development of corneal disease was impaired in ΔexoS, ΔexoT, and ΔexoST mutants of both strains, but not in a ΔexoY mutant. ΔexoST mutants were also rapidly killed in neutrophils in vitro and were impaired in their ability to promote neutrophil apoptosis in vivo compared with PAO1. Point mutations in the ADP ribosyltransferase (ADPR) regions of ExoS or ExoT also impaired proapoptotic activity in infected neutrophils, and exoST(ADPR-) mutants replicated the ΔexoST phenotype in vitro and in vivo, whereas mutations in rho-GTPase-activating protein showed the same phenotype as PAO1. Together, these findings demonstrate that the pathogenesis of P. aeruginosa keratitis in ExoS- and ExoT-producing strains is almost entirely due to their ADPR activities, which subvert the host response by targeting the antibacterial activity of infiltrating neutrophils.
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.