ArticleMedical microbiology and immunology2010
Pro-autophagic signal induction by bacterial pore-forming toxins.
Article in Medical microbiology and immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 81 citations in OpenAlex.
- Article
- Epsilon toxin induces cytotoxicity by mediating autophagy and apoptosis via the PI3K/AKT/mTOR signaling pathway in A549 cells.Molecular biology reports · 2025Article
- Mechanisms ofFrontiers in cellular and infection microbiology · 2025Review
- An Update on the Study of the Molecular Mechanisms Involved in Autophagy during Bacterial Pathogenesis.Biomedicines · 2024Review
- Cellular Stress Responses against Coronavirus Infection: A Means of the Innate Antiviral Defense.Journal of microbiology and biotechnology · 2024Review
- The role of autophagy in tick-endosymbiont interactions: insights fromMicrobiology spectrum · 2024Article
- Phenol-Soluble Modulin α3 Stimulates Autophagy in HaCaT Keratinocytes.Biomedicines · 2023Article
- C. elegans monitor energy status via the AMPK pathway to trigger innate immune responses against bacterial pathogens.Communications biology · 2022Article
- Biting the hand that feeds: Metabolic determinants of cell fate during infection.Frontiers in immunology · 2022Review
- Review
- Autophagy-based unconventional secretion of HMGB1 by keratinocytes plays a pivotal role in psoriatic skin inflammation.Autophagy · 2021Article
- Hiding in Plain Sight: Formation and Function of Stress Granules During Microbial Infection of Mammalian Cells.Frontiers in molecular biosciences · 2021Review
- Innate immunity in C. elegans.Current topics in developmental biology · 2021Review
- Protein Kinase R in Bacterial Infections: Friend or Foe?Frontiers in immunology · 2021Review
- Making the Most of the Host; Targeting the Autophagy Pathway FacilitatesFrontiers in immunology · 2021Review
- Interaction of Macrophages and Cholesterol-Dependent Cytolysins: The Impact on Immune Response and Cellular Survival.Toxins · 2020Review
- Evaluation of the in vitro Function of Platelet Concentrates from Pooled Buffy Coats or Apheresis.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2020Article
- Review
- Mechanisms protecting host cells against bacterial pore-forming toxins.Cellular and molecular life sciences : CMLS · 2019Review
- GCN2 controls the cellular checkpoint: potential target for regulating inflammation.Cell death discovery · 2018Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pore-forming toxins (PFT) comprise a large, structurally heterogeneous group of bacterial protein toxins. Nucleated target cells mount complex responses which allow them to survive moderate membrane damage by PFT. Autophagy has recently been implicated in responses to various PFT, but how this process is triggered is not known, and the significance of the phenomenon is not understood. Here, we show that S. aureus α-toxin, Vibrio cholerae cytolysin, streptolysin O and E. coli haemolysin activate two pathways leading to autophagy. The first pathway is triggered via AMP-activated protein kinase (AMPK). AMPK is a major energy sensor which induces autophagy by inhibiting the target of rapamycin complex 1 (TORC1) in response to a drop of the cellular ATP/AMP-ratio, as is also observed in response to membrane perforation. The second pathway is activated by the conserved eIF2α-kinase GCN2, which causes global translational arrest and promotes autophagy in response to starvation. The latter could be accounted for by impaired amino acid transport into target cells. Notably, PKR, an eIF2α-kinase which has been implicated in autophagy induction during viral infection, was also activated upon membrane perforation, and evidence was obtained that phosphorylation of eIF2α is required for the accumulation of autophagosomes in α-toxin-treated cells. Treatment with 3-methyl-adenine inhibited autophagy and disrupted the ability of cells to recover from sublethal attack by S. aureus α-toxin. We propose that PFT induce pro-autophagic signals through membrane perforation-dependent nutrient and energy depletion, and that an important function of autophagy in this context is to maintain metabolic homoeostasis.
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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.