ArticlePLoS pathogens2014
The Pseudomonas aeruginosa type III translocon is required for biofilm formation at the epithelial barrier.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
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- Alizarin, which reduces ExoS, attenuates inflammation by P. aeruginosa in H292 cells.Journal of microbiology (Seoul, Korea) · 2025Article
- BIChromET: A Chromogenic Culture Medium for Detection of Piperacillin/Tazobactam and Cefepime Resistance inAntibiotics (Basel, Switzerland) · 2023Article
- Revisiting Host-Pathogen Interactions in Cystic Fibrosis Lungs in the Era of CFTR Modulators.International journal of molecular sciences · 2023Review
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- Elevated c-di-GMP Levels and Expression of the Type III Secretion System Promote Corneal Infection by Pseudomonas aeruginosa.Infection and immunity · 2022Article
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- BosR: A novel biofilm-specific regulator inFrontiers in microbiology · 2022Article
- Molecular Mechanisms Involved in Pseudomonas aeruginosa Bacteremia.Advances in experimental medicine and biology · 2022Review
- The Small RNA ErsA Impacts the Anaerobic Metabolism ofFrontiers in microbiology · 2021Article
- The Small RNA ErsA Plays a Role in the Regulatory Network of Pseudomonas aeruginosa Pathogenicity in Airway Infections.mSphere · 2020Article
- Cystic fibrosis transmembrane conductance regulator dysfunction in platelets drives lung hyperinflammation.The Journal of clinical investigation · 2020Article
- TheApplied and environmental microbiology · 2019Article
- Neutrophil Extracellular Traps Confine Pseudomonas aeruginosa Ocular Biofilms and Restrict Brain Invasion.Cell host & microbe · 2019Article
- Mouse model of Gram-negative prosthetic joint infection reveals therapeutic targets.JCI insight · 2018Article
- Construction and evaluation of type III secretion system mutants of the catfish pathogen Edwardsiella piscicida.Journal of fish diseases · 2018Article
- Maladaptive role of neutrophil extracellular traps in pathogen-induced lung injury.JCI insight · 2018Article
- Targeting the Mucosal Barrier: How Pathogens Modulate the Cellular Polarity Network.Cold Spring Harbor perspectives in biology · 2017Review
- Antimicrobial efficacy against Pseudomonas aeruginosa biofilm formation in a three-dimensional lung epithelial model and the influence of fetal bovine serum.Scientific reports · 2017Article
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8 authors at 5 institutions in 4 countries.
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Abstract
Clinical infections by Pseudomonas aeruginosa, a deadly Gram-negative, opportunistic pathogen of immunocompromised hosts, often involve the formation of antibiotic-resistant biofilms. Although biofilm formation has been extensively studied in vitro on glass or plastic surfaces, much less is known about biofilm formation at the epithelial barrier. We have previously shown that when added to the apical surface of polarized epithelial cells, P. aeruginosa rapidly forms cell-associated aggregates within 60 minutes of infection. By confocal microscopy we now show that cell-associated aggregates exhibit key characteristics of biofilms, including the presence of extracellular matrix and increased resistance to antibiotics compared to planktonic bacteria. Using isogenic mutants in the type III secretion system, we found that the translocon, but not the effectors themselves, were required for cell-associated aggregation on the surface of polarized epithelial cells and at early time points in a murine model of acute pneumonia. In contrast, the translocon was not required for aggregation on abiotic surfaces, suggesting a novel function for the type III secretion system during cell-associated aggregation. Supernatants from epithelial cells infected with wild-type bacteria or from cells treated with the pore-forming toxin streptolysin O could rescue aggregate formation in a type III secretion mutant, indicating that cell-associated aggregation requires one or more host cell factors. Our results suggest a previously unappreciated function for the type III translocon in the formation of P. aeruginosa biofilms at the epithelial barrier and demonstrate that biofilms may form at early time points of infection.
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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.