ArticleThe Journal of experimental medicine1998
Yersinia enterocolitica impairs activation of transcription factor NF-kappaB: involvement in the induction of programmed cell death and in the suppression of the macrophage tumor necrosis factor alpha production.
Article in The Journal of experimental medicine, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 239 citations in OpenAlex.
- Molecular mechanisms of co-infections.EMBO reports · 2025Review
- Blockade of IKK signaling induces RIPK1-independent apoptosis in human macrophages.PLoS pathogens · 2024Article
- Roles of RIPK1 as a stress sentinel coordinating cell survival and immunogenic cell death.Nature reviews. Molecular cell biology · 2023Review
- Reprogramming of Cell Death Pathways by Bacterial Effectors as a Widespread Virulence Strategy.Infection and immunity · 2022Review
- Heightened Virulence ofInfection and immunity · 2021Article
- Galectin-1 Cooperates with Yersinia Outer Protein (Yop) P to Thwart Protective Immunity by Repressing Nitric Oxide Production.Biomolecules · 2021Article
- The role of nuclear factor kappa B (NF-κB) in filarial pathology.Journal of cell communication and signaling · 2021Review
- Lung Macrophage Functional Properties in Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2020Review
- Article
- RIPK1-dependent apoptosis bypasses pathogen blockade of innate signaling to promote immune defense.The Journal of experimental medicine · 2017Article
- Outer Membrane Protein 25 ofFrontiers in veterinary science · 2017Article
- Cell-Extrinsic TNF Collaborates with TRIF Signaling To Promote Yersinia-Induced Apoptosis.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Yersinia virulence factors - a sophisticated arsenal for combating host defences.F1000Research · 2016Review
- The apoptogenic toxin AIP56 is a metalloprotease A-B toxin that cleaves NF-κb P65.PLoS pathogens · 2013Article
- Article
- Subversion of inflammasome activation and pyroptosis by pathogenic bacteria.Frontiers in cellular and infection microbiology · 2013Review
- Modulation of host immune defenses by Aeromonas and Yersinia species: convergence on toxins secreted by various secretion systems.Frontiers in cellular and infection microbiology · 2013Article
- TLR2 signaling subpathways regulate TLR9 signaling for the effective induction of IL-12 upon stimulation by heat-killed Brucella abortus.Cellular & molecular immunology · 2012Article
- Aeromonas salmonicida-secreted protein AopP is a potent inducer of apoptosis in a mammalian and a Drosophila model.Cellular microbiology · 2012Article
- Cell death programs in Yersinia immunity and pathogenesis.Frontiers in cellular and infection microbiology · 2012Review
20 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
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we investigated the activity of transcription factor NF-kappaB in macrophages infected with Yersinia enterocolitica. Although triggering initially a weak NF-kappaB signal, Y. enterocolitica inhibited NF-kappaB activation in murine J774A.1 and peritoneal macrophages within 60 to 90 min. Simultaneously, Y. enterocolitica prevented prolonged degradation of the inhibitory proteins IkappaB-alpha and IkappaB-beta observed by treatment with lipopolysaccharide (LPS) or nonvirulent, plasmid-cured yersiniae. Analysis of different Y. enterocolitica mutants revealed a striking correlation between the abilities of these strains to inhibit NF-kappaB and to suppress the tumor necrosis factor alpha (TNF-alpha) production as well as to trigger macrophage apoptosis. When NF-kappaB activation was prevented by the proteasome inhibitor MG-132, nonvirulent yersiniae as well as LPS became able to trigger J774A.1 cell apoptosis and inhibition of the TNF-alpha secretion. Y. enterocolitica also impaired the activity of NF-kappaB in epithelial HeLa cells. Although neither Y. enterocolitica nor TNF-alpha could induce HeLa cell apoptosis alone, TNF-alpha provoked apoptosis when activation of NF-kappaB was inhibited by Yersinia infection or by the proteasome inhibitor MG-132. Together, these data demonstrate that Y. enterocolitica suppresses cellular activation of NF-kappaB, which inhibits TNF-alpha release and triggers apoptosis in macrophages. Our results also suggest that Yersinia infection confers susceptibility to programmed cell death to other cell types, provided that the appropriate death signal is delivered.
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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.