ArticleInfection and immunity2001
Fas (CD95)-Fas ligand interactions are responsible for monocyte apoptosis occurring as a result of phagocytosis and killing of Staphylococcus aureus.
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 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 64 citations in OpenAlex.
- FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025Review
- Shaping of the alveolar landscape by respiratory infections and long-term consequences for lung immunity.Frontiers in immunology · 2023Review
- Lung Macrophage Functional Properties in Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2020Review
- Reduced internalization of TNF-ɑ/TNFR1 down-regulates caspase dependent phagocytosis induced cell death (PICD) in neonatal monocytes.PloS one · 2017Article
- Fas ligand-expressing lymphocytes enhance alveolar macrophage apoptosis in the resolution of acute pulmonary inflammation.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Allogeneic haematopoietic stem cell transplantation as therapy for chronic granulomatous disease--single centre experience.Journal of clinical immunology · 2011Article
- ADAM17 activity and other mechanisms of soluble L-selectin production during death receptor-induced leukocyte apoptosis.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Akt and SHIP modulate Francisella escape from the phagosome and induction of the Fas-mediated death pathway.PloS one · 2009Article
- Interaction of human peripheral blood monocytes with apoptotic polymorphonuclear cells.Immunology · 2009Article
- Leptospira interrogans induces apoptosis in macrophages via caspase-8- and caspase-3-dependent pathways.Infection and immunity · 2009Article
- Article
- Phagocytosis of Borrelia burgdorferi, the Lyme disease spirochete, potentiates innate immune activation and induces apoptosis in human monocytes.Infection and immunity · 2008Article
- Article
- Tumour-derived microvesicles carry several surface determinants and mRNA of tumour cells and transfer some of these determinants to monocytes.Cancer immunology, immunotherapy : CII · 2006Article
- Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity.Current immunology reviews · 2006Article
- Staphylococcus aureus Panton-Valentine leukocidin directly targets mitochondria and induces Bax-independent apoptosis of human neutrophils.The Journal of clinical investigation · 2005Article
- Caspase-8 activation precedes alterations of mitochondrial membrane potential during monocyte apoptosis induced by phagocytosis and killing of Staphylococcus aureus.Infection and immunity · 2004Article
- Augmentation of NKT and NK cell-mediated cytotoxicity by peptidoglycan monomer linked with zinc.Mediators of inflammation · 2002Article
- alpha-Toxin is a mediator of Staphylococcus aureus-induced cell death and activates caspases via the intrinsic death pathway independently of death receptor signaling.The Journal of cell biology · 2001Article
- Fas and Fas ligand immunolocalization in pancreatic islets of NOD mice during spontaneous and cyclophosphamide-accelerated diabetes.The Histochemical journalArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human peripheral blood monocytes become apoptotic following phagocytosis of Staphylococcus aureus. In this study, we investigated the mechanisms involved in this phenomenon. Cells exposed to bacteria were examined for the surface expression of Fas and Fas ligand (FasL). The level of soluble form of FasL was also measured in the culture supernatants. As Fas-mediated apoptosis involves the activation of caspases, the activities of caspase-8 and caspase-3 were determined. Finally, the involvement of oxidative stress in apoptosis of infected monocytes was investigated. The data indicated that as a consequence of phagocytosis of S. aureus, FasL is released from the monocyte surface and induces apoptosis of phagocytic monocytes and to some extent the bystander cells. The importance of this mechanism was confirmed by demonstrating that blockage of CD95 prevents S. aureus-induced apoptosis of monocytes. Cell death occurring after phagocytosis of S. aureus involves the activation of caspase-3-like proteases, as the specific caspase-3 inhibitor suppressed apoptosis of infected cells. The generation of reactive oxygen intermediates by phagocytic monocytes by itself is not sufficient as a death signal but rather acts in up-regulating FasL shedding and possibly in modulating caspase activity.
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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.