ArticleInfection and immunity2001
Pseudomonas aeruginosa-induced apoptosis involves mitochondria and stress-activated protein kinases.
Article in Infection and immunity, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 85 citations in OpenAlex.
- Bacterial extracellular vesicles in colorectal cancer: mechanisms, biomarker potential, and therapeutic engineering.Cell communication and signaling : CCS · 2026Review
- FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025Review
- Bacterial Infections Affect Male Fertility: A Focus on the Oxidative Stress-Autophagy Axis.Frontiers in cell and developmental biology · 2021Review
- Integrated evaluation of lung disease in single animals.PloS one · 2021Article
- Mitochondrial Stress Responses and "Mito-Inflammation" in Cystic Fibrosis.Frontiers in pharmacology · 2020Review
- Selective delivery of T22-PE24-H6 to CXCR4Theranostics · 2020Article
- Cathelicidin is a "fire alarm", generating protective NLRP3-dependent airway epithelial cell inflammatory responses during infection with Pseudomonas aeruginosa.PLoS pathogens · 2019Article
- Uncovering effects of antibiotics on the host and microbiota using transkingdom gene networks.Gut · 2015Article
- The impact of simvastatin on pulmonary effectors of Pseudomonas aeruginosa infection.PloS one · 2014Article
- The opportunistic pathogen Pseudomonas aeruginosa activates the DNA double-strand break signaling and repair pathway in infected cells.Cellular and molecular life sciences : CMLS · 2013Article
- Article
- CFTR activity and mitochondrial function.Redox biology · 2013Review
- Monitoring mitochondrial inner membrane potential for detecting early changes in viability of bacterium-infected human bone marrow-derived mesenchymal stem cells.Stem cell research & therapy · 2012Article
- Host DNA repair proteins in response to Pseudomonas aeruginosa in lung epithelial cells and in mice.Infection and immunity · 2011Article
- The role of sphingolipids and ceramide in pulmonary inflammation in cystic fibrosis.The open respiratory medicine journal · 2010Article
- Pseudomonas aeruginosa: mannose sensitive hemagglutinin inhibits the growth of human hepatocarcinoma cells via mannose-mediated apoptosis.Digestive diseases and sciences · 2009Article
- Comparison of gene expression profiles of conjunctival cell lines with primary cultured conjunctival epithelial cells and human conjunctival tissue.Gene expression · 2009Article
- Phospholipase A2 functions in Pseudomonas aeruginosa-induced apoptosis.Infection and immunity · 2006Article
- Pathogen-host interactions in Pseudomonas aeruginosa pneumonia.American journal of respiratory and critical care medicine · 2005Review
- Downregulation of mitogen-activated protein kinases by the Bordetella bronchiseptica Type III secretion system leads to attenuated nonclassical macrophage activation.Infection and immunity · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pseudomonas aeruginosa, a gram-negative facultative pathogen, causes severe infections in immunocompromised and cystic fibrosis patients. However, the molecular details of the interaction between P. aeruginosa and mammalian cells are still largely unknown. Here we demonstrate that infection of human conjunctiva epithelial Chang cells with the well-characterized P. aeruginosa strain PAO-I results in rapid induction of apoptosis. Apoptosis was mediated by mitochondrial alterations, in particular mitochondrial depolarization, synthesis of reactive oxygen intermediates, and release of cytochrome c, as well as an activation of Jun N-terminal kinases (JNK). Stimulation of these events was dependent on upregulation of CD95 on infected cells, and a deficiency of CD95 or the CD95 ligand prevented mitochondrial changes, JNK activation, and apoptosis upon infection. Further, efficient apoptosis of Chang epithelial cells required infection with live P. aeruginosa, adhesion but not invasion of the bacteria, and expression of the type III secretion system in PAO-I. The data indicate a type III secretion system-dependent, sequential activation of several signaling pathways by P. aeruginosa PAO-I, resulting in apoptosis of the infected cell.
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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.