ArticlePLoS pathogens2007
Macrophage activation redirects yersinia-infected host cell death from apoptosis to caspase-1-dependent pyroptosis.
Article in PLoS pathogens, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.
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Who cites it
142 citing papers in PubMed, 243 citations in OpenAlex.
- Kinetic control of macrophage death by PTM-turnover crosstalk in infection and inflammation.Cell chemical biology · 2026Review
- Ferroptosis in biliary tract cancer: Molecular mechanisms and therapeutic applications (Review).International journal of oncology · 2026Review
- Ebselen, a promising host-directed therapeutic option againstFrontiers in microbiology · 2026Article
- Anti-infective compounds forSustainable microbiology · 2026Review
- Unraveling the Pathogenetic Potential and Immune Crosstalk of Yersinia spp. in Inflammatory Bowel Disease.Journal of immunology research · 2026Review
- Molecular mechanisms of immune cell death in immunosenescence.Cell death and differentiation · 2025Review
- Nigericin Induces Paraptosis-Like Cell Death Instead of Pyroptosis in Corneal Keratocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Alzheimer's disease neuropathology and its estimation with fluid and imaging biomarkers.Molecular neurodegeneration · 2025Review
- Regulated cell death and its role in Alzheimer's disease and amyotrophic lateral sclerosis.Acta neuropathologica · 2024Review
- Parkinson's disease models and death signaling: what do we know until now?Frontiers in neuroanatomy · 2024Review
- ASC/inflammasome-independent pyroptosis in ovarian cancer cells through translational augmentation of caspase-1.iScience · 2023Article
- Human umbilical cord mesenchymal stem cell exosomes alleviate acute kidney injury by inhibiting pyroptosis in rats and NRK-52E cells.Renal failure · 2023Article
- A Review on Caspases: Key Regulators of Biological Activities and Apoptosis.Molecular neurobiology · 2023Review
- Article
- Knockdown of NADPH oxidase 4 reduces mitochondrial oxidative stress and neuronal pyroptosis following intracerebral hemorrhage.Neural regeneration research · 2023Article
- Programmed Cell Death Pathways in Cholangiocarcinoma: Opportunities for Targeted Therapy.Cancers · 2023Review
- Article
- Neutrophil inflammasomes sense the subcellular delivery route of translocated bacterial effectors and toxins.Cell reports · 2022Article
- Review
- A pyroptosis-associated signature plays a role in prognosis prediction in clear cell renal cell carcinoma.BMC medical genomics · 2022Article
82 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Infection of macrophages by Yersinia species results in YopJ-dependent apoptosis, and naïve macrophages are highly susceptible to this form of cell death. Previous studies have demonstrated that macrophages activated with lipopolysaccharide (LPS) prior to infection are resistant to YopJ-dependent cell death; we found this simultaneously renders macrophages susceptible to killing by YopJ(-) Yersinia pseudotuberculosis (Yptb). YopJ(-) Yptb-induced macrophage death was dependent on caspase-1 activation, resulting in rapid permeability to small molecules, followed by membrane breakdown and DNA damage, and accompanied by cleavage and release of proinflammatory interleukin-18. Induction of caspase-1-dependent death, or pyroptosis, required the bacterial type III translocon but none of its known translocated proteins. Wild-type Yptb infection also triggered pyroptosis: YopJ-dependent activation of proapoptotic caspase-3 was significantly delayed in activated macrophages and resulted in caspase-1-dependent pyroptosis. The transition to susceptibility was not limited to LPS activation; it was also seen in macrophages activated with other Toll-like receptor (TLR) ligands and intact nonviable bacteria. Yptb infection triggered macrophage activation and activation of caspase-1 in vivo. Y. pestis infection of activated macrophages also stimulated caspase-1 activation. These results indicate that host signaling triggered by TLR and other activating ligands during the course of Yersinia infection redirects both the mechanism of host cell death and the downstream consequences of death by shifting from noninflammatory apoptosis to inflammatory pyroptosis.
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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.