ArticleCell death and differentiation2022
Mitochondria supply sub-lethal signals for cytokine secretion and DNA-damage in H. pylori infection.
Article in Cell death and differentiation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Evasion of cell death despite mitochondrial outer membrane permeabilization: an oncogenic outcome of apoptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- The second mitochondrial activator of caspases (SMAC) regulates growth, inflammation and mitochondrial integrity in cancer cells.Cell death and differentiation · 2026Article
- MTCH2 promotes BAX and BAK self-assembly and apoptotic pore growth.Nature structural & molecular biology · 2026Article
- What does BCL-2 do? From new molecular insights to the clinical implications.Cell death and differentiation · 2026Review
- Mitochondrial Stress inAntioxidants (Basel, Switzerland) · 2026Review
- Mitochondrial Dysfunction is a Crucial Immune Checkpoint for Neuroinflammation and Neurodegeneration: mtDAMPs in Focus.Molecular neurobiology · 2025Review
- Article
- NMolecular biotechnology · 2024Article
- Mitochondria and cell death.Nature cell biology · 2024Review
- NOD1 and NOD2: Essential Monitoring Partners in the Innate Immune System.Current issues in molecular biology · 2024Review
- The caspase-activated DNase promotes cellular senescence.The EMBO journal · 2024Article
- The Caspase-Activated DNase drives inflammation and contributes to defense against viral infection.Cell death and differentiation · 2024Article
- Mechanisms of BCL-2 family proteins in mitochondrial apoptosis.Nature reviews. Molecular cell biology · 2023Review
- Programmed Cell Death Pathways in Cholangiocarcinoma: Opportunities for Targeted Therapy.Cancers · 2023Review
- Mitochondrial control of inflammation.Nature reviews. Immunology · 2023Review
- Mitochondria and cell death-associated inflammation.Cell death and differentiation · 2023Review
- Sub-lethal signals in the mitochondrial apoptosis apparatus: pernicious by-product or physiological event?Cell death and differentiation · 2023Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
15 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The bacterium Helicobacter pylori induces gastric inflammation and predisposes to cancer. H. pylori-infected epithelial cells secrete cytokines and chemokines and undergo DNA-damage. We show that the host cell's mitochondrial apoptosis system contributes to cytokine secretion and DNA-damage in the absence of cell death. H. pylori induced secretion of cytokines/chemokines from epithelial cells, dependent on the mitochondrial apoptosis machinery. A signalling step was identified in the release of mitochondrial Smac/DIABLO, which was required for alternative NF-κB-activation and contributed to chemokine secretion. The bacterial cag-pathogenicity island and bacterial muropeptide triggered mitochondrial host cell signals through the pattern recognition receptor NOD1. H. pylori-induced DNA-damage depended on mitochondrial apoptosis signals and the caspase-activated DNAse. In biopsies from H. pylori-positive patients, we observed a correlation of Smac-levels and inflammation. Non-apoptotic cells in these samples showed evidence of caspase-3-activation, correlating with phosphorylation of the DNA-damage response kinase ATM. Thus, H. pylori activates the mitochondrial apoptosis pathway to a sub-lethal level. During infection, Smac has a cytosolic, pro-inflammatory role in the absence of apoptosis. Further, DNA-damage through sub-lethal mitochondrial signals is likely to contribute to mutagenesis and cancer development.
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