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Toll-like receptors expressed on embryonic macrophages couple inflammatory signals to iron metabolism during early ontogenesis
J. Balounová, T. Vavrochová, M. Benešová, O. Ballek, M. Kolář, D. Filipp,
Jazyk angličtina Země Německo
Typ dokumentu časopisecké články, práce podpořená grantem
Odkazy
PubMed
24470066
DOI
10.1002/eji.201344040
Knihovny.cz E-zdroje
- MeSH
- diferenciační antigeny genetika imunologie metabolismus MeSH
- embryo savčí cytologie imunologie metabolismus MeSH
- makrofágy cytologie imunologie metabolismus MeSH
- myši knockoutované MeSH
- myši MeSH
- protein MyD88 genetika imunologie metabolismus MeSH
- signální transdukce fyziologie MeSH
- toll-like receptor 2 genetika imunologie metabolismus MeSH
- vývojová regulace genové exprese genetika imunologie MeSH
- zánět genetika imunologie MeSH
- železo imunologie metabolismus MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Mammalian TLRs in adult animals serve indispensable functions in establishing innate and adaptive immunity and contributing to the homeostasis of surrounding tissues. However, the expression and function of TLRs during mammalian embryonic development has not been studied so far. Here, we show that CD45(+) CD11b(+) F4/80(+) macrophages from 10.5-day embryo (E10.5) co-express TLRs and CD14. These macrophages, which have the capability to engulf both apoptotic cells and bacteria, secrete a broad spectrum of proinflammatory cytokines and chemokines upon TLR stimulation, demonstrating that their TLRs are functional. Comparative microarray analysis revealed an additional set of genes that were significantly upregulated in E10.5 TLR2(+) CD11b(+) macrophages. This analysis, together with our genetic, microscopic, and biochemical evidence, showed that embryonic phagocytes express protein machinery that is essential for the recycling of cellular iron and that this expression can be regulated by TLR engagement in a MyD88-dependent manner, leading to typical inflammatory M1 responses. These results characterize the utility of TLRs as suitable markers for early embryonic phagocytes as well as molecular triggers of cellular responses, the latter being demonstrated by the involvement of TLRs in an inflammation-mediated regulation of embryonic homeostasis via iron metabolism.
Department of Cell Biology Faculty of Science Charles University Prague Prague Czech Republic
Laboratory of Immunobiology Institute of Molecular Genetics AS CR Prague Czech Republic
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- $a Mammalian TLRs in adult animals serve indispensable functions in establishing innate and adaptive immunity and contributing to the homeostasis of surrounding tissues. However, the expression and function of TLRs during mammalian embryonic development has not been studied so far. Here, we show that CD45(+) CD11b(+) F4/80(+) macrophages from 10.5-day embryo (E10.5) co-express TLRs and CD14. These macrophages, which have the capability to engulf both apoptotic cells and bacteria, secrete a broad spectrum of proinflammatory cytokines and chemokines upon TLR stimulation, demonstrating that their TLRs are functional. Comparative microarray analysis revealed an additional set of genes that were significantly upregulated in E10.5 TLR2(+) CD11b(+) macrophages. This analysis, together with our genetic, microscopic, and biochemical evidence, showed that embryonic phagocytes express protein machinery that is essential for the recycling of cellular iron and that this expression can be regulated by TLR engagement in a MyD88-dependent manner, leading to typical inflammatory M1 responses. These results characterize the utility of TLRs as suitable markers for early embryonic phagocytes as well as molecular triggers of cellular responses, the latter being demonstrated by the involvement of TLRs in an inflammation-mediated regulation of embryonic homeostasis via iron metabolism.
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