Vitamin D3 down‐regulates monocyte TLR expression and triggers hyporesponsiveness to pathogen‐associated molecular patterns
Toll‐like receptors (TLR) represent an ancient front‐line defence system that enables the host organism to sense the presence of microbial components within minutes. As inducers of inflammation, TLR act as important triggers of distinct entities such as sepsis or autoimmune disease exacerbation. We...
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| Veröffentlicht in: | European Journal of Immunology 2006-02, Vol.36 (2), p.361-370 |
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| creator | Sadeghi, Kambis Wessner, Barbara Laggner, Ute Ploder, Martin Tamandl, Dietmar Friedl, Josef Zügel, Ullrich Steinmeyer, Andreas Pollak, Arnold Roth, Erich Boltz‐Nitulescu, George Spittler, Andreas |
| description | Toll‐like receptors (TLR) represent an ancient front‐line defence system that enables the host organism to sense the presence of microbial components within minutes. As inducers of inflammation, TLR act as important triggers of distinct entities such as sepsis or autoimmune disease exacerbation. We report here that vitamin D3 [1α,25‐dihydroxycholecalciferol, 1,25(OH)2D3] suppresses the expression of TLR2 and TLR4 protein and mRNA in human monocytes in a time‐ and dose‐dependent fashion. Despite 1,25(OH)2D3‐induced up‐regulation of CD14, challenge of human monocytes with either LPS or lipoteichoic acid resulted in impaired TNF‐α and procoagulatory tissue factor (CD142) production, emphasizing the critical role of TLR in the induction of inflammation. Moreover, reduced TLR levels in 1,25(OH)2D3‐treated phagocytes were accompanied by impaired NF‐κB/RelA translocation to the nucleus and by reduced p38 and p42/44 (extracellular signal‐regulated kinase 1/2) phosphorylation upon TLR‐ligand engagement. Both TLR down‐regulation and CD14 up‐regulation were substantially inhibited by the vitamin D receptor (VDR) antagonist ZK 159222, indicating that the immunomodulatory effect of 1,25(OH)2D3 on innate immunity receptors requires VDR transcription factor activation. Our data provide strong evidence that 1,25(OH)2D3 primes monocytes to respond less effectively to bacterial cell wall components in a VDR‐dependent mechanism, most likely due to decreased levels of TLR2 and TLR4. |
| doi_str_mv | 10.1002/eji.200425995 |
| format | Article |
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As inducers of inflammation, TLR act as important triggers of distinct entities such as sepsis or autoimmune disease exacerbation. We report here that vitamin D3 [1α,25‐dihydroxycholecalciferol, 1,25(OH)2D3] suppresses the expression of TLR2 and TLR4 protein and mRNA in human monocytes in a time‐ and dose‐dependent fashion. Despite 1,25(OH)2D3‐induced up‐regulation of CD14, challenge of human monocytes with either LPS or lipoteichoic acid resulted in impaired TNF‐α and procoagulatory tissue factor (CD142) production, emphasizing the critical role of TLR in the induction of inflammation. Moreover, reduced TLR levels in 1,25(OH)2D3‐treated phagocytes were accompanied by impaired NF‐κB/RelA translocation to the nucleus and by reduced p38 and p42/44 (extracellular signal‐regulated kinase 1/2) phosphorylation upon TLR‐ligand engagement. Both TLR down‐regulation and CD14 up‐regulation were substantially inhibited by the vitamin D receptor (VDR) antagonist ZK 159222, indicating that the immunomodulatory effect of 1,25(OH)2D3 on innate immunity receptors requires VDR transcription factor activation. Our data provide strong evidence that 1,25(OH)2D3 primes monocytes to respond less effectively to bacterial cell wall components in a VDR‐dependent mechanism, most likely due to decreased levels of TLR2 and TLR4.</description><identifier>ISSN: 0014-2980</identifier><identifier>EISSN: 1521-4141</identifier><identifier>EISSN: 1365-2567</identifier><identifier>DOI: 10.1002/eji.200425995</identifier><identifier>PMID: 16402404</identifier><language>eng</language><publisher>Weinheim: WILEY‐VCH Verlag</publisher><subject>Active Transport, Cell Nucleus - drug effects ; Active Transport, Cell Nucleus - immunology ; Calcitriol - analogs & derivatives ; Calcitriol - pharmacology ; Cells, Cultured ; Cholecalciferol - immunology ; Cholecalciferol - pharmacology ; Dose-Response Relationship, Drug ; Down-Regulation - drug effects ; Down-Regulation - immunology ; Human ; Humans ; Inflammation ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation - pathology ; Lipopolysaccharide ; Lipopolysaccharide Receptors - biosynthesis ; Lipopolysaccharide Receptors - immunology ; Lipopolysaccharides - immunology ; Lipopolysaccharides - pharmacology ; Macrophage Activation - drug effects ; Macrophage Activation - immunology ; Mitogen-Activated Protein Kinase 1 - immunology ; Mitogen-Activated Protein Kinase 1 - metabolism ; Monocytes - immunology ; Monocytes - metabolism ; Monocytes - pathology ; Monocytes/macrophages ; p38 Mitogen-Activated Protein Kinases - immunology ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phosphorylation - drug effects ; Receptors, Calcitriol - antagonists & inhibitors ; Receptors, Calcitriol - immunology ; Receptors, Calcitriol - metabolism ; Signal Transduction - drug effects ; Signal Transduction - immunology ; Teichoic Acids - immunology ; Teichoic Acids - pharmacology ; TLR ; Toll-Like Receptor 2 - biosynthesis ; Toll-Like Receptor 2 - immunology ; Toll-Like Receptor 4 - biosynthesis ; Toll-Like Receptor 4 - immunology ; Transcription Factor RelA - immunology ; Transcription Factor RelA - metabolism ; Up-Regulation - drug effects ; Up-Regulation - immunology</subject><ispartof>European Journal of Immunology, 2006-02, Vol.36 (2), p.361-370</ispartof><rights>Copyright © 2006 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4755-84f4e5506e51a6fc29c9664e6813bbbb7434d74faca79db7af72d41c83ece84f3</citedby><cites>FETCH-LOGICAL-c4755-84f4e5506e51a6fc29c9664e6813bbbb7434d74faca79db7af72d41c83ece84f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Feji.200425995$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Feji.200425995$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16402404$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sadeghi, Kambis</creatorcontrib><creatorcontrib>Wessner, Barbara</creatorcontrib><creatorcontrib>Laggner, Ute</creatorcontrib><creatorcontrib>Ploder, Martin</creatorcontrib><creatorcontrib>Tamandl, Dietmar</creatorcontrib><creatorcontrib>Friedl, Josef</creatorcontrib><creatorcontrib>Zügel, Ullrich</creatorcontrib><creatorcontrib>Steinmeyer, Andreas</creatorcontrib><creatorcontrib>Pollak, Arnold</creatorcontrib><creatorcontrib>Roth, Erich</creatorcontrib><creatorcontrib>Boltz‐Nitulescu, George</creatorcontrib><creatorcontrib>Spittler, Andreas</creatorcontrib><title>Vitamin D3 down‐regulates monocyte TLR expression and triggers hyporesponsiveness to pathogen‐associated molecular patterns</title><title>European Journal of Immunology</title><addtitle>Eur J Immunol</addtitle><description>Toll‐like receptors (TLR) represent an ancient front‐line defence system that enables the host organism to sense the presence of microbial components within minutes. As inducers of inflammation, TLR act as important triggers of distinct entities such as sepsis or autoimmune disease exacerbation. We report here that vitamin D3 [1α,25‐dihydroxycholecalciferol, 1,25(OH)2D3] suppresses the expression of TLR2 and TLR4 protein and mRNA in human monocytes in a time‐ and dose‐dependent fashion. Despite 1,25(OH)2D3‐induced up‐regulation of CD14, challenge of human monocytes with either LPS or lipoteichoic acid resulted in impaired TNF‐α and procoagulatory tissue factor (CD142) production, emphasizing the critical role of TLR in the induction of inflammation. Moreover, reduced TLR levels in 1,25(OH)2D3‐treated phagocytes were accompanied by impaired NF‐κB/RelA translocation to the nucleus and by reduced p38 and p42/44 (extracellular signal‐regulated kinase 1/2) phosphorylation upon TLR‐ligand engagement. Both TLR down‐regulation and CD14 up‐regulation were substantially inhibited by the vitamin D receptor (VDR) antagonist ZK 159222, indicating that the immunomodulatory effect of 1,25(OH)2D3 on innate immunity receptors requires VDR transcription factor activation. Our data provide strong evidence that 1,25(OH)2D3 primes monocytes to respond less effectively to bacterial cell wall components in a VDR‐dependent mechanism, most likely due to decreased levels of TLR2 and TLR4.</description><subject>Active Transport, Cell Nucleus - drug effects</subject><subject>Active Transport, Cell Nucleus - immunology</subject><subject>Calcitriol - analogs & derivatives</subject><subject>Calcitriol - pharmacology</subject><subject>Cells, Cultured</subject><subject>Cholecalciferol - immunology</subject><subject>Cholecalciferol - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Down-Regulation - drug effects</subject><subject>Down-Regulation - immunology</subject><subject>Human</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - immunology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Lipopolysaccharide</subject><subject>Lipopolysaccharide Receptors - biosynthesis</subject><subject>Lipopolysaccharide Receptors - immunology</subject><subject>Lipopolysaccharides - immunology</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Macrophage Activation - drug effects</subject><subject>Macrophage Activation - immunology</subject><subject>Mitogen-Activated Protein Kinase 1 - immunology</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Monocytes - immunology</subject><subject>Monocytes - metabolism</subject><subject>Monocytes - pathology</subject><subject>Monocytes/macrophages</subject><subject>p38 Mitogen-Activated Protein Kinases - immunology</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phosphorylation - drug effects</subject><subject>Receptors, Calcitriol - antagonists & inhibitors</subject><subject>Receptors, Calcitriol - immunology</subject><subject>Receptors, Calcitriol - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - immunology</subject><subject>Teichoic Acids - immunology</subject><subject>Teichoic Acids - pharmacology</subject><subject>TLR</subject><subject>Toll-Like Receptor 2 - biosynthesis</subject><subject>Toll-Like Receptor 2 - immunology</subject><subject>Toll-Like Receptor 4 - biosynthesis</subject><subject>Toll-Like Receptor 4 - immunology</subject><subject>Transcription Factor RelA - immunology</subject><subject>Transcription Factor RelA - metabolism</subject><subject>Up-Regulation - drug effects</subject><subject>Up-Regulation - immunology</subject><issn>0014-2980</issn><issn>1521-4141</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkT1PwzAQhi0EgvIxsiJPbAHbsZ14RFC-VAkJAWvkOpdilMTBToFuIPED-I38ElxawQa33En33DPci9AuJQeUEHYID_aAEcKZUEqsoAEVjCaccrqKBoRQnjCVkw20GcIDIURJodbRBpWcME74AL3d2V43tv18fT9Jceme4_ThYTKtdQ8BN651ZtYDvhldY3jpPIRgXYt1W-Le28kEfMD3s87FRefaYJ-gjQjuHe50f-8mMPfpEJyxUVhGYQ0myv1834NvwzZaq3QdYGfZt9Dt6fDm-DwZXZ1dHB-NEsMzIZKcVxyEIBIE1bIyTBklJQeZ03QcK-MpLzNeaaMzVY4zXWWs5NTkKRiIx-kW2l94O-8epxD6orHBQF3rFtw0FFRJFX8i_wczRvL0G0wWoPEuBA9V0XnbaD8rKCnm4RQxnOInnMjvLcXTcQPlL71MIwLZAni2Ncz-thXDy4tf9Rf-I6FR</recordid><startdate>200602</startdate><enddate>200602</enddate><creator>Sadeghi, Kambis</creator><creator>Wessner, Barbara</creator><creator>Laggner, Ute</creator><creator>Ploder, Martin</creator><creator>Tamandl, Dietmar</creator><creator>Friedl, Josef</creator><creator>Zügel, Ullrich</creator><creator>Steinmeyer, Andreas</creator><creator>Pollak, Arnold</creator><creator>Roth, Erich</creator><creator>Boltz‐Nitulescu, George</creator><creator>Spittler, Andreas</creator><general>WILEY‐VCH Verlag</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7T5</scope><scope>C1K</scope><scope>H94</scope></search><sort><creationdate>200602</creationdate><title>Vitamin D3 down‐regulates monocyte TLR expression and triggers hyporesponsiveness to pathogen‐associated molecular patterns</title><author>Sadeghi, Kambis ; 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As inducers of inflammation, TLR act as important triggers of distinct entities such as sepsis or autoimmune disease exacerbation. We report here that vitamin D3 [1α,25‐dihydroxycholecalciferol, 1,25(OH)2D3] suppresses the expression of TLR2 and TLR4 protein and mRNA in human monocytes in a time‐ and dose‐dependent fashion. Despite 1,25(OH)2D3‐induced up‐regulation of CD14, challenge of human monocytes with either LPS or lipoteichoic acid resulted in impaired TNF‐α and procoagulatory tissue factor (CD142) production, emphasizing the critical role of TLR in the induction of inflammation. Moreover, reduced TLR levels in 1,25(OH)2D3‐treated phagocytes were accompanied by impaired NF‐κB/RelA translocation to the nucleus and by reduced p38 and p42/44 (extracellular signal‐regulated kinase 1/2) phosphorylation upon TLR‐ligand engagement. Both TLR down‐regulation and CD14 up‐regulation were substantially inhibited by the vitamin D receptor (VDR) antagonist ZK 159222, indicating that the immunomodulatory effect of 1,25(OH)2D3 on innate immunity receptors requires VDR transcription factor activation. Our data provide strong evidence that 1,25(OH)2D3 primes monocytes to respond less effectively to bacterial cell wall components in a VDR‐dependent mechanism, most likely due to decreased levels of TLR2 and TLR4.</abstract><cop>Weinheim</cop><pub>WILEY‐VCH Verlag</pub><pmid>16402404</pmid><doi>10.1002/eji.200425995</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | Wiley Free Content; MEDLINE; IngentaConnect Free/Open Access Journals; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Active Transport, Cell Nucleus - drug effects Active Transport, Cell Nucleus - immunology Calcitriol - analogs & derivatives Calcitriol - pharmacology Cells, Cultured Cholecalciferol - immunology Cholecalciferol - pharmacology Dose-Response Relationship, Drug Down-Regulation - drug effects Down-Regulation - immunology Human Humans Inflammation Inflammation - immunology Inflammation - metabolism Inflammation - pathology Lipopolysaccharide Lipopolysaccharide Receptors - biosynthesis Lipopolysaccharide Receptors - immunology Lipopolysaccharides - immunology Lipopolysaccharides - pharmacology Macrophage Activation - drug effects Macrophage Activation - immunology Mitogen-Activated Protein Kinase 1 - immunology Mitogen-Activated Protein Kinase 1 - metabolism Monocytes - immunology Monocytes - metabolism Monocytes - pathology Monocytes/macrophages p38 Mitogen-Activated Protein Kinases - immunology p38 Mitogen-Activated Protein Kinases - metabolism Phosphorylation - drug effects Receptors, Calcitriol - antagonists & inhibitors Receptors, Calcitriol - immunology Receptors, Calcitriol - metabolism Signal Transduction - drug effects Signal Transduction - immunology Teichoic Acids - immunology Teichoic Acids - pharmacology TLR Toll-Like Receptor 2 - biosynthesis Toll-Like Receptor 2 - immunology Toll-Like Receptor 4 - biosynthesis Toll-Like Receptor 4 - immunology Transcription Factor RelA - immunology Transcription Factor RelA - metabolism Up-Regulation - drug effects Up-Regulation - immunology |
| title | Vitamin D3 down‐regulates monocyte TLR expression and triggers hyporesponsiveness to pathogen‐associated molecular patterns |
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