ArticleInnate immunity2019
Pyocyanin induces NK92 cell apoptosis via mitochondrial damage and elevated intracellular Ca
Article in Innate immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 11 citations in OpenAlex.
- Mechanisms of Mitochondrial Toxicity and Cytotoxicity Caused by Pseudomonas aeruginosa Pyocyanin in Human Nasal Epithelial Cells.International forum of allergy & rhinology · 2026Article
- Anti-pyocyanin Antibody Exhibits Cytotoxicity Protective Effects on Macrophages: A Promising Innovative Therapeutic Approach forACS pharmacology & translational science · 2025Article
- Modulation of pulmonary immune functions by theFrontiers in immunology · 2025Review
- Reactive oxygen species drive foraging decisions in Caenorhabditis elegans.Redox biology · 2023Article
- Mitochondrial Reactive Oxygen Species: Double-Edged Weapon in Host Defense and Pathological Inflammation During Infection.Frontiers in immunology · 2020Review
- The protective effects of antigen-specific IgY on pyocyanin-treated human lymphoma Raji cells.F1000Research · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudomonas aeruginosa-derived pigment pyocyanin (PCN) has been proved to induce cell apoptosis mediated by the generation of reactive oxygen species (ROS), which has been studied mainly in epithelial cells and neutrophils. However, we previously found that the PCN-producing strain PA14 induces cell apoptosis in human NK cell line NK92 more effectively than in PCN-deficient strain PA14-phZ1/2 via a yet undetermined mechanism. In the current study, we found that PCN-induced NK92 cell apoptosis occurs through mitochondrial damage despite inhibiting intracellular ROS generation. Intracellular Ca
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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.