Enteropathogenic Escherichia coli Uses NleA to Inhibit NLRP3 Inflammasome Activation
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Summary
These findings provide the first example of EPEC-mediated suppression of inflammasome activity in which NieA plays a novel role in controlling the host immune response through targeting of NLRP3.
- Type
- article
- Published
- 2015-09-01
- Cited by
- 96
- References
- 49
- Access
- Open access
- OpenAlex
- https://openalex.org/W1689514240
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:32489549
Keywords
Inflammasome, Enteropathogenic Escherichia coli, Effector, Microbiology, Secretion
References
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- Caspase‐1‐dependent pore formation during pyroptosis leads to osmotic lysis of infected host macrophages
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- A C‐terminal class I PDZ binding motif of EspI/NleA modulates the virulence of attaching and effacing Escherichia coli and Citrobacter rodentium
- The bacterial virulence factor NleA inhibits cellular protein secretion by disrupting mammalian COPII function.
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- Toll-like receptor signalling
- NleC, a Type III Secretion Protease, Compromises NF-κB Activation by Targeting p65/RelA
- TRIF Licenses Caspase-11-Dependent NLRP3 Inflammasome Activation by Gram-Negative Bacteria
- Crystal Structure of Procaspase-1 Zymogen Domain Reveals Insight into Inflammatory Caspase Autoactivation
- The Type III Effectors NleE and NleB from Enteropathogenic E. coli and OspZ from Shigella Block Nuclear Translocation of NF-κB p65
Cited by
- Immunity and Tolerance Induced by Intestinal Mucosal Dendritic Cells
- Regulation of inflammasomes by ubiquitination
- The Genetics of Enteropathogenic Escherichia coli Virulence.
- Evasion and interference: intracellular pathogens modulate caspase-dependent inflammatory responses
- Identification of the Q969R gain-of-function polymorphism in the gene encoding porcine NLRP3 and its distribution in pigs of Asian and European origin
- Enhanced Survival of Rifampin- and Streptomycin-Resistant Escherichia coli Inside Macrophages
- Deubiquitinases: Novel Therapeutic Targets in Immune Surveillance?
- The Type Three Secretion System 2-Encoded Regulator EtrB Modulates Enterohemorrhagic Escherichia coli Virulence Gene Expression
- Modulation of the Inflammasome Signaling Pathway by Enteropathogenic and Enterohemorrhagic Escherichia coli
- Tight Junction Disruption Induced by Type 3 Secretion System Effectors Injected by Enteropathogenic and Enterohemorrhagic Escherichia coli
- Bacterial Virulence Factor Inhibits Caspase-4/11 Activation in Intestinal Epithelial Cells
- Deviant Behavior: Tick-Borne Pathogens and Inflammasome Signaling
- Modulation of host signaling in the inflammatory response by enteropathogenic Escherichia coli virulence proteins
- Bacterial secretion systems and regulation of inflammasome activation
- The Bacterial T6SS Effector EvpP Prevents NLRP3 Inflammasome Activation by Inhibiting the Ca2+-Dependent MAPK-Jnk Pathway.
- Delivery systems for antimicrobial peptides.
- Generation of enteropathogenic E. coli strains lacking the repertoire of effectors translocated by the type III protein secretion system and their characterization in the infection of cultured cell lines and human intestinal biopsies
- Determining the protective effects of lactobacillus reuteri against enteropathogenic escherichia coli infection
- Molecular cloning and characterization of DNGR‐1 in rhesus macaques
- Commensal-to-pathogen transition: One-single transposon insertion results in two pathoadaptive traits in Escherichia coli -macrophage interaction
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