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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
2010-11-2
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pubmed:abstractText |
Wnt/Frizzled signaling, essential for embryonic development, has also recently been implicated in the modulation of inflammatory processes. In the current study, we observed a reciprocal regulation of the Toll-like receptor (TLR)/nuclear factor-?B (NF-?B) and the Wnt/?-catenin pathway after aerosol infection of mice with Mycobacterium tuberculosis: whereas proinflammatory mediators were substantially increased, ?-catenin signaling was significantly reduced. A systematic screen of Fzd homologs in infected mice identified Fzd1 mRNA to be significantly up-regulated during the course of infection. In vitro infection of murine macrophages led to a strong induction of Fzd1 that was dependent on TLRs, the myeloid differentiation response gene 88 (MyD88), and a functional NF-?B pathway. Flow cytometry demonstrated an elevated Fzd1 expression on macrophages in response to M. tuberculosis that was synergistically enhanced in the presence of IFN-?. Addition of the Fzd1 ligand Wnt3a induced Wnt/?-catenin signaling in murine macrophages that was inhibited in the presence of a soluble Fzd1/Fc fusion protein. Furthermore, Wnt3a reduced TNF release, suggesting that Wnt3a promotes anti-inflammatory functions in murine macrophages. The current data support the notion that evolutionarily conserved Wnt/Fzd signaling is involved in balancing the inflammatory response to microbial stimulation of innate immune cells of vertebrate origin.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Biological Markers,
http://linkedlifedata.com/resource/pubmed/chemical/Frizzled Receptors,
http://linkedlifedata.com/resource/pubmed/chemical/Fzd1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, G-Protein-Coupled,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Wnt Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Wnt3 Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Wnt3A Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Wnt3a protein, mouse
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1530-6860
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
4599-612
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:20667980-Animals,
pubmed-meshheading:20667980-Biological Markers,
pubmed-meshheading:20667980-Frizzled Receptors,
pubmed-meshheading:20667980-Gene Expression Regulation,
pubmed-meshheading:20667980-Ligands,
pubmed-meshheading:20667980-Lung,
pubmed-meshheading:20667980-Macrophages,
pubmed-meshheading:20667980-Mice,
pubmed-meshheading:20667980-Mice, Inbred C57BL,
pubmed-meshheading:20667980-Mice, Knockout,
pubmed-meshheading:20667980-Mycobacterium tuberculosis,
pubmed-meshheading:20667980-NF-kappa B,
pubmed-meshheading:20667980-RNA, Messenger,
pubmed-meshheading:20667980-Receptors, G-Protein-Coupled,
pubmed-meshheading:20667980-Recombinant Fusion Proteins,
pubmed-meshheading:20667980-Signal Transduction,
pubmed-meshheading:20667980-Tuberculosis,
pubmed-meshheading:20667980-Tumor Necrosis Factors,
pubmed-meshheading:20667980-Up-Regulation,
pubmed-meshheading:20667980-Wnt Proteins,
pubmed-meshheading:20667980-Wnt3 Protein,
pubmed-meshheading:20667980-Wnt3A Protein
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pubmed:year |
2010
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pubmed:articleTitle |
Frizzled1 is a marker of inflammatory macrophages, and its ligand Wnt3a is involved in reprogramming Mycobacterium tuberculosis-infected macrophages.
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pubmed:affiliation |
Division of Microbial Interface Biology, Research Center Borstel, Borstel, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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