Activation of B cell apoptotic pathways in the course of Francisella tularensis infection
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
20600796
DOI
10.1016/j.micpath.2010.06.003
PII: S0882-4010(10)00105-1
Knihovny.cz E-zdroje
- MeSH
- apoptóza * MeSH
- B-lymfocyty mikrobiologie MeSH
- buněčné linie MeSH
- cytochromy c metabolismus MeSH
- Francisella tularensis patogenita MeSH
- kaspasa 3 biosyntéza MeSH
- kaspasa 8 biosyntéza MeSH
- kaspasa 9 biosyntéza MeSH
- lidé MeSH
- membránový potenciál mitochondrií MeSH
- mitochondrie enzymologie fyziologie MeSH
- protein Bid biosyntéza MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- BID protein, human MeSH Prohlížeč
- CASP8 protein, human MeSH Prohlížeč
- cytochromy c MeSH
- kaspasa 3 MeSH
- kaspasa 8 MeSH
- kaspasa 9 MeSH
- protein Bid MeSH
Francisella tularensis is a facultative intracellular, gram-negative bacterium that induces apoptosis in macrophages and B cells. Here we show apoptotic pathways that are activated in the Ramos human B cell line in the course of F. tularensis infection. Live bacteria F. tularensis FSC200 activate caspases 8, 9 and 3, as well as Bid; release cytochrome c and apoptosis-inducing factor from mitochondria; and induce depolarization of mitochondrial membrane potential in the Ramos cell line, thus leading these cells to apoptosis. Unlike live bacteria, killed F. tularensis FSC200 bacteria activated only caspase 3, and did not cause apoptosis of Ramos cells as measured by annexin V. Killed bacteria also caused accumulation of anti-apoptotic protein Bclx(L) in mitochondrial membranes. Thus, live F. tularensis activates both caspase pathways (receptor-mediated and intrinsic) as well as caspase-independent mitochondrial death.
Citace poskytuje Crossref.org
