ArticleNature microbiology2019
TesG is a type I secretion effector of Pseudomonas aeruginosa that suppresses the host immune response during chronic infection.
Article in Nature microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
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- Advances in Tetrahedral Framework Nucleic Acids (tFNAs) for Lung Injury Repair: Mechanisms, Therapeutic Applications, and Future Directions.International journal of nanomedicine · 2026Review
- Host miRNA orchestration of mitophagy pathways during bacterial infection: current advances and future directions.Frontiers in microbiology · 2026Review
- Multi-omics profiling of acuteVirulence · 2025Article
- ThemSphere · 2025Article
- Intranasal phage therapy overcomes antibody neutralization challenges in pulmonary Pseudomonas aeruginosa infections.Archives of microbiology · 2025Article
- tesG expression as a potential clinical biomarker for chronic Pseudomonas aeruginosa pulmonary biofilm infections.BMC medicine · 2025Article
- Hybrid Cell Membrane-Engineered Nanocarrier for Triple-Action Strategy to Address Pseudomonas aeruginosa Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Correlation Analysis Between Multi-Drug Resistance Phenotype and Virulence Factor Expression of ClinicalCurrent issues in molecular biology · 2025Article
- Framework nucleic acid strategy enables closer microbial contact for programming short-range interaction.Science advances · 2024Article
- Co-immunization with DNA vaccines encoding yidR and IL-17 augments host immune response againstVirulence · 2024Article
- Furazolidone reduces the pathogenesis ofHeliyon · 2024Article
- Phenotypic heterogeneity unveils a negative correlation between antibiotic resistance and quorum sensing inFrontiers in microbiology · 2024Article
- A Bacterial Quorum Sensing Regulated Protease Inhibits Host Immune Responses by Cleaving Death Domains of Innate Immune Adaptors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Evolution of lasR mutants in polymorphic Pseudomonas aeruginosa populations facilitates chronic infection of the lung.Nature communications · 2023Article
- Chronic pulmonary bacterial infection facilitates breast cancer lung metastasis by recruiting tumor-promoting MHCIISignal transduction and targeted therapy · 2023Article
- An integrated multi-omics analysis of identifies distinct molecular characteristics in pulmonary infections of Pseudomonas aeruginosa.PLoS pathogens · 2023Article
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Authors and funding
21 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudomonas aeruginosa is a versatile Gram-negative pathogen with intricate intracellular regulatory networks that enable it to adapt to and flourish in a variety of biotic and abiotic habitats. However, the mechanism permitting the persistent survival of P. aeruginosa within host tissues and causing chronic symptoms still remains largely elusive. By using in situ RNA sequencing, here we show that P. aeruginosa adopts different metabolic pathways and virulence repertoires to dominate the progression of acute and chronic lung infections. Notably, a virulence factor named TesG, which is controlled by the vital quorum-sensing system and secreted by the downstream type I secretion system, can suppress the host inflammatory response and facilitate the development of chronic lung infection. Mechanically, TesG can enter the intracellular compartment of macrophages through clathrin-mediated endocytosis, competitively inhibit the activity of eukaryotic small GTPase and thus suppress subsequent neutrophil influx, cell cytoskeletal rearrangement of macrophages and the secretion of cytokines and chemokines. Therefore, the identification of TesG in this study reveals a type I secretion apparatus of P. aeruginosa that functions during the host-pathogen interaction, and may open an avenue for the further mechanistic study of chronic respiratory diseases and the development of antibacterial therapy.
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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.