ArticleInfection and immunity2013
Flagellar motility is a key determinant of the magnitude of the inflammasome response to Pseudomonas aeruginosa.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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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.
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Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
- Indole-Acetic Acid Impairs Pseudomonas aeruginosa Virulence and Alters Lung Infection in Mice.MicrobiologyOpen · 2025Article
- Flagellum-deficientMicrobiology spectrum · 2024Article
- Amino Acid-Induced Chemotaxis Plays a Key Role in the Adaptation ofMicroorganisms · 2024Article
- Assessment of the Glycan-Binding Profile of Pseudomonas aeruginosa PAO1.Microbiology spectrum · 2023Article
- Assessment of the Glycan-Binding Profile ofbioRxiv : the preprint server for biology · 2023Article
- Chemical Optimization of SelectiveACS infectious diseases · 2023Article
- Caspase-1-driven neutrophil pyroptosis and its role in host susceptibility to Pseudomonas aeruginosa.PLoS pathogens · 2022Article
- Zinc Exposure Promotes Commensal-to-Pathogen Transition inInternational journal of molecular sciences · 2021Article
- Article
- Review
- Identification of cell-surface glycans that mediate motility-dependent binding and internalization of Pseudomonas aeruginosa by phagocytes.Molecular immunology · 2021Article
- Review
- IRF8 Regulates Gram-Negative Bacteria-Mediated NLRP3 Inflammasome Activation and Cell Death.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Distinct Contributions of CD18 Integrins for Binding and Phagocytic Internalization of Pseudomonas aeruginosa.Infection and immunity · 2020Article
- Cystic Fibrosis and Pseudomonas aeruginosa: the Host-Microbe Interface.Clinical microbiology reviews · 2019Review
- Phosphatidylinositol-(3,4,5)-Trisphosphate Induces Phagocytosis of Nonmotile Pseudomonas aeruginosa.Infection and immunity · 2018Article
- Acidosis exacerbates in vivo IL-1-dependent inflammatory responses and neutrophil recruitment during pulmonary Pseudomonas aeruginosa infection.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Guanylate binding proteins facilitate caspase-11-dependent pyroptosis in response to type 3 secretion system-negativeCell death discovery · 2018Article
- Review
- The effect of loss of O-antigen ligase on phagocytic susceptibility of motile and non-motile Pseudomonas aeruginosa.Molecular immunology · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
We previously demonstrated that bacterial flagellar motility is a fundamental mechanism by which host phagocytes bind and ingest bacteria. Correspondingly, loss of bacterial motility, consistently observed in clinical isolates from chronic Pseudomonas aeruginosa infections, enables bacteria to evade association and ingestion of P. aeruginosa by phagocytes both in vitro and in vivo. Since bacterial interactions with the phagocyte cell surface are required for type three secretion system-dependent NLRC4 inflammasome activation by P. aeruginosa, we hypothesized that reduced bacterial association with phagocytes due to loss of bacterial motility, independent of flagellar expression, will lead to reduced inflammasome activation. Here we report that inflammasome activation is reduced in response to nonmotile P. aeruginosa. Nonmotile P. aeruginosa elicits reduced IL-1β production as well as caspase-1 activation by peritoneal macrophages and bone marrow-derived dendritic cells in vitro. Importantly, nonmotile P. aeruginosa also elicits reduced IL-1β levels in vivo in comparison to those elicited by wild-type P. aeruginosa. This is the first demonstration that loss of bacterial motility results in reduced inflammasome activation and antibacterial IL-1β host response. These results provide a critical insight into how the innate immune system responds to bacterial motility and, correspondingly, how pathogens have evolved mechanisms to evade the innate immune system.
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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.