ArticleScientific reports2018
Bacterial Pore-Forming Toxins Promote the Activation of Caspases in Parallel to Necroptosis to Enhance Alarmin Release and Inflammation During Pneumonia.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- Alterations in nutrient availability in the lungs duringInfection and immunity · 2025Article
- Alleviating penicillin-resistant Streptococcus pneumoniae‑induced lung epithelial cell injury: mechanistic insights into effects of the optimized combination of main components from Yinhuapinggan granules.BMC infectious diseases · 2025Article
- Induction of Paraptotic Cell Death in Cancer Cells by Triptycene-Peptide Hybrids and the Revised Mechanism of Paraptosis II.Biochemistry · 2024Article
- Targeting necroptosis: a promising avenue for respiratory disease treatment.Cell communication and signaling : CCS · 2024Review
- The dance of macrophage death: the interplay between the inevitable and the microenvironment.Frontiers in immunology · 2024Review
- Major adverse cardiovascular events are associated with necroptosis during severe COVID-19.Critical care (London, England) · 2023Observational
- Acute organ injury and long-term sequelae of severe pneumococcal infections.Pneumonia (Nathan Qld.) · 2023Review
- Pneumolysin promotes host cell necroptosis and bacterial competence during pneumococcal meningitis as shown by whole-animal dual RNA-seq.Cell reports · 2022Article
- A Jack of All Trades: The Role of Pneumococcal Surface Protein A in the Pathogenesis ofFrontiers in cellular and infection microbiology · 2022Review
- Panorama of the Intracellular Molecular Concert Orchestrated by Actinoporins, Pore-Forming Toxins from Sea Anemones.Toxins · 2021Review
- The Natterin Proteins Diversity: A Review on Phylogeny, Structure, and Immune Function.Toxins · 2021Review
- Streptococcus pneumoniae binds to host GAPDH on dying lung epithelial cells worsening secondary infection following influenza.Cell reports · 2021Article
- IGF2BP2 knockdown inhibits LPS-induced pyroptosis in BEAS-2B cells by targeting caspase 4, a crucial molecule of the non-canonical pyroptosis pathway.Experimental and therapeutic medicine · 2021Article
- Streptococcus pneumoniae Binds to Host Lactate Dehydrogenase via PspA and PspC To Enhance Virulence.mBio · 2021Article
- Pulmonary Macrophage Cell Death in Lung Health and Disease.American journal of respiratory cell and molecular biology · 2021Review
- A surfactant polymer wound dressing protects human keratinocytes from inducible necroptosis.Scientific reports · 2021Article
- RIPK protein kinase family: Atypical lives of typical kinases.Seminars in cell & developmental biology · 2021Review
- Necroptosis in Pulmonary Diseases: A New Therapeutic Target.Frontiers in pharmacology · 2021Review
- An in vivo atlas of host-pathogen transcriptomes duringProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Inhibition of Necroptosis to Prevent Long-term Cardiac Damage During Pneumococcal Pneumonia and Invasive Disease.The Journal of infectious diseases · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Pore-forming toxins are the most common virulence factor in pathogenic bacteria. They lead to membrane permeabilization and cell death. Herein, we show that respiratory epithelial cells (REC) undergoing bacterial pore-forming toxin (PFT)-induced necroptosis simultaneously experienced caspase activation independently of RIPK3. MLKL deficient REC treated with a pan-caspase inhibitor were protected in an additive manner against PFT-induced death. Subsequently, cleaved versions of caspases-2, -4 and -10 were detected within REC undergoing necroptosis by immunoblots and monoclonal antibody staining. Caspase activation was observed in lung samples from mice and non-human primates experiencing Gram-negative and Gram-positive bacterial pneumonia, respectively. During apoptosis, caspase activation normally leads to cell shrinkage, nuclear condensation, and immunoquiescent death. In contrast, caspase activity during PFT-induced necroptosis increased the release of alarmins to the extracellular milieu. Caspase-mediated alarmin release was found sufficient to activate resting macrophages, leading to Interleukin-6 production. In a mouse model of Gram-negative pneumonia, deletion of caspases -2 and -11, the mouse orthologue of caspase-4, reduced pulmonary inflammation, immune cell infiltration and lung damage. Thus, our study describes a previously unrecognized role for caspase activation in parallel to necroptosis, and indicates that their activity plays a critical pro-inflammatory role during bacterial pneumonia.
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