Francisella tularensis strain LVS resides in MHC II-positive autophagic vacuoles in macrophages
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
18450226
DOI
10.1007/bf02932193
Knihovny.cz E-resources
- MeSH
- Autophagy * MeSH
- Cell Line MeSH
- Microscopy, Fluorescence MeSH
- PTEN Phosphohydrolase analysis MeSH
- Francisella tularensis immunology MeSH
- Cathepsin D analysis MeSH
- Microscopy, Confocal MeSH
- Macrophages microbiology MeSH
- Histocompatibility Antigens Class II analysis MeSH
- Mice MeSH
- Tumor Suppressor Protein p53 analysis MeSH
- Microtubule-Associated Proteins analysis MeSH
- Vacuoles chemistry microbiology MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- PTEN Phosphohydrolase MeSH
- Cathepsin D MeSH
- Map1lc3b protein, mouse MeSH Browser
- Histocompatibility Antigens Class II MeSH
- Tumor Suppressor Protein p53 MeSH
- Microtubule-Associated Proteins MeSH
- Pten protein, mouse MeSH Browser
The Francisella tularensis strain LVS phagosome disintegrates during the first few hours after bacterial entry and microbes are released to the cytosol. Within 12 h both rapid multiplication of microbes and a steep increase of apoptosis of infected macrophages occur. We searched for signals involved in the death of macrophages and detected molecules associated with the autophagy machinery cathepsin D, PTEN, p53 and LC3, whose levels or modification were influenced by ongoing in vitro tularemic infection. The sequestration of cytoplasmic F. tularensis LVS into autophagosomes was confirmed by co-localization of the LVS strain containing vacuoles with LC3 (an autophagosomal marker). We also demonstrated the presence of MHC II antigens in these autophagosomes, indicating that they might act as a source of endogenous tularemic antigens for presentation to CD4+ T lymphocytes.
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