RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner
<p<Abstract</p< <p<Background</p< <p<The receptor for advanced glycation endproducts, RAGE, is involved in the pathogenesis of many inflammatory conditions, which is mostly related to its strong activation of NF-κB but also due to its function as ligand for the β<sub...
Ausführliche Beschreibung
Autor*in: |
Nawroth Peter P [verfasserIn] Lange-Sperandio Baerbel [verfasserIn] Tschada Raphaela [verfasserIn] Zablotskaya Victoria [verfasserIn] Buschmann Kirsten [verfasserIn] Dannenberg Susanne [verfasserIn] Kamphues Anna [verfasserIn] Frommhold David [verfasserIn] Poeschl Johannes [verfasserIn] Bierhaus Angelika [verfasserIn] Sperandio Markus [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2011 |
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Übergeordnetes Werk: |
In: BMC Immunology - BMC, 2003, 12(2011), 1, p 56 |
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Übergeordnetes Werk: |
volume:12 ; year:2011 ; number:1, p 56 |
Links: |
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DOI / URN: |
10.1186/1471-2172-12-56 |
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Katalog-ID: |
DOAJ033675716 |
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520 | |a <p<Abstract</p< <p<Background</p< <p<The receptor for advanced glycation endproducts, RAGE, is involved in the pathogenesis of many inflammatory conditions, which is mostly related to its strong activation of NF-κB but also due to its function as ligand for the β<sub<2</sub<-integrin Mac-1. To further dissect the stimulus-dependent role of RAGE on leukocyte recruitment during inflammation, we investigated β<sub<2</sub<-integrin-dependent leukocyte adhesion in <it<RAGE<sup<-/- </sup<</it<and <it<Icam1<sup<-/- </sup<</it<mice in different cremaster muscle models of inflammation using intravital microscopy.</p< <p<Results</p< <p<We demonstrate that RAGE, but not ICAM-1 substantially contributes to N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced leukocyte adhesion in TNF-α-pretreated cremaster muscle venules in a Mac-1-dependent manner. In contrast, fMLP-stimulated leukocyte adhesion in unstimulated cremaster muscle venules is independent of RAGE, but dependent on ICAM-1 and its interaction with LFA-1. Furthermore, chemokine CXCL1-stimulated leukocyte adhesion in surgically prepared cremaster muscle venules was independent of RAGE but strongly dependent on ICAM-1 and LFA-1 suggesting a differential and stimulus-dependent regulation of leukocyte adhesion during inflammation in vivo.</p< <p<Conclusion</p< <p<Our results demonstrate that RAGE and ICAM-1 differentially regulate leukocyte adhesion in vivo in a stimulus-dependent manner.</p< | ||
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10.1186/1471-2172-12-56 doi (DE-627)DOAJ033675716 (DE-599)DOAJ4e39400ea15a445bb664d5c1e75a985e DE-627 ger DE-627 rakwb eng RC581-607 Nawroth Peter P verfasserin aut RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The receptor for advanced glycation endproducts, RAGE, is involved in the pathogenesis of many inflammatory conditions, which is mostly related to its strong activation of NF-κB but also due to its function as ligand for the β<sub<2</sub<-integrin Mac-1. To further dissect the stimulus-dependent role of RAGE on leukocyte recruitment during inflammation, we investigated β<sub<2</sub<-integrin-dependent leukocyte adhesion in <it<RAGE<sup<-/- </sup<</it<and <it<Icam1<sup<-/- </sup<</it<mice in different cremaster muscle models of inflammation using intravital microscopy.</p< <p<Results</p< <p<We demonstrate that RAGE, but not ICAM-1 substantially contributes to N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced leukocyte adhesion in TNF-α-pretreated cremaster muscle venules in a Mac-1-dependent manner. In contrast, fMLP-stimulated leukocyte adhesion in unstimulated cremaster muscle venules is independent of RAGE, but dependent on ICAM-1 and its interaction with LFA-1. Furthermore, chemokine CXCL1-stimulated leukocyte adhesion in surgically prepared cremaster muscle venules was independent of RAGE but strongly dependent on ICAM-1 and LFA-1 suggesting a differential and stimulus-dependent regulation of leukocyte adhesion during inflammation in vivo.</p< <p<Conclusion</p< <p<Our results demonstrate that RAGE and ICAM-1 differentially regulate leukocyte adhesion in vivo in a stimulus-dependent manner.</p< Immunologic diseases. Allergy Lange-Sperandio Baerbel verfasserin aut Tschada Raphaela verfasserin aut Zablotskaya Victoria verfasserin aut Buschmann Kirsten verfasserin aut Dannenberg Susanne verfasserin aut Kamphues Anna verfasserin aut Frommhold David verfasserin aut Poeschl Johannes verfasserin aut Bierhaus Angelika verfasserin aut Sperandio Markus verfasserin aut In BMC Immunology BMC, 2003 12(2011), 1, p 56 (DE-627)326644962 (DE-600)2041500-X 14712172 nnns volume:12 year:2011 number:1, p 56 https://doi.org/10.1186/1471-2172-12-56 kostenfrei https://doaj.org/article/4e39400ea15a445bb664d5c1e75a985e kostenfrei http://www.biomedcentral.com/1471-2172/12/56 kostenfrei https://doaj.org/toc/1471-2172 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2011 1, p 56 |
spelling |
10.1186/1471-2172-12-56 doi (DE-627)DOAJ033675716 (DE-599)DOAJ4e39400ea15a445bb664d5c1e75a985e DE-627 ger DE-627 rakwb eng RC581-607 Nawroth Peter P verfasserin aut RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The receptor for advanced glycation endproducts, RAGE, is involved in the pathogenesis of many inflammatory conditions, which is mostly related to its strong activation of NF-κB but also due to its function as ligand for the β<sub<2</sub<-integrin Mac-1. To further dissect the stimulus-dependent role of RAGE on leukocyte recruitment during inflammation, we investigated β<sub<2</sub<-integrin-dependent leukocyte adhesion in <it<RAGE<sup<-/- </sup<</it<and <it<Icam1<sup<-/- </sup<</it<mice in different cremaster muscle models of inflammation using intravital microscopy.</p< <p<Results</p< <p<We demonstrate that RAGE, but not ICAM-1 substantially contributes to N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced leukocyte adhesion in TNF-α-pretreated cremaster muscle venules in a Mac-1-dependent manner. In contrast, fMLP-stimulated leukocyte adhesion in unstimulated cremaster muscle venules is independent of RAGE, but dependent on ICAM-1 and its interaction with LFA-1. Furthermore, chemokine CXCL1-stimulated leukocyte adhesion in surgically prepared cremaster muscle venules was independent of RAGE but strongly dependent on ICAM-1 and LFA-1 suggesting a differential and stimulus-dependent regulation of leukocyte adhesion during inflammation in vivo.</p< <p<Conclusion</p< <p<Our results demonstrate that RAGE and ICAM-1 differentially regulate leukocyte adhesion in vivo in a stimulus-dependent manner.</p< Immunologic diseases. Allergy Lange-Sperandio Baerbel verfasserin aut Tschada Raphaela verfasserin aut Zablotskaya Victoria verfasserin aut Buschmann Kirsten verfasserin aut Dannenberg Susanne verfasserin aut Kamphues Anna verfasserin aut Frommhold David verfasserin aut Poeschl Johannes verfasserin aut Bierhaus Angelika verfasserin aut Sperandio Markus verfasserin aut In BMC Immunology BMC, 2003 12(2011), 1, p 56 (DE-627)326644962 (DE-600)2041500-X 14712172 nnns volume:12 year:2011 number:1, p 56 https://doi.org/10.1186/1471-2172-12-56 kostenfrei https://doaj.org/article/4e39400ea15a445bb664d5c1e75a985e kostenfrei http://www.biomedcentral.com/1471-2172/12/56 kostenfrei https://doaj.org/toc/1471-2172 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2011 1, p 56 |
allfields_unstemmed |
10.1186/1471-2172-12-56 doi (DE-627)DOAJ033675716 (DE-599)DOAJ4e39400ea15a445bb664d5c1e75a985e DE-627 ger DE-627 rakwb eng RC581-607 Nawroth Peter P verfasserin aut RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The receptor for advanced glycation endproducts, RAGE, is involved in the pathogenesis of many inflammatory conditions, which is mostly related to its strong activation of NF-κB but also due to its function as ligand for the β<sub<2</sub<-integrin Mac-1. To further dissect the stimulus-dependent role of RAGE on leukocyte recruitment during inflammation, we investigated β<sub<2</sub<-integrin-dependent leukocyte adhesion in <it<RAGE<sup<-/- </sup<</it<and <it<Icam1<sup<-/- </sup<</it<mice in different cremaster muscle models of inflammation using intravital microscopy.</p< <p<Results</p< <p<We demonstrate that RAGE, but not ICAM-1 substantially contributes to N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced leukocyte adhesion in TNF-α-pretreated cremaster muscle venules in a Mac-1-dependent manner. In contrast, fMLP-stimulated leukocyte adhesion in unstimulated cremaster muscle venules is independent of RAGE, but dependent on ICAM-1 and its interaction with LFA-1. Furthermore, chemokine CXCL1-stimulated leukocyte adhesion in surgically prepared cremaster muscle venules was independent of RAGE but strongly dependent on ICAM-1 and LFA-1 suggesting a differential and stimulus-dependent regulation of leukocyte adhesion during inflammation in vivo.</p< <p<Conclusion</p< <p<Our results demonstrate that RAGE and ICAM-1 differentially regulate leukocyte adhesion in vivo in a stimulus-dependent manner.</p< Immunologic diseases. Allergy Lange-Sperandio Baerbel verfasserin aut Tschada Raphaela verfasserin aut Zablotskaya Victoria verfasserin aut Buschmann Kirsten verfasserin aut Dannenberg Susanne verfasserin aut Kamphues Anna verfasserin aut Frommhold David verfasserin aut Poeschl Johannes verfasserin aut Bierhaus Angelika verfasserin aut Sperandio Markus verfasserin aut In BMC Immunology BMC, 2003 12(2011), 1, p 56 (DE-627)326644962 (DE-600)2041500-X 14712172 nnns volume:12 year:2011 number:1, p 56 https://doi.org/10.1186/1471-2172-12-56 kostenfrei https://doaj.org/article/4e39400ea15a445bb664d5c1e75a985e kostenfrei http://www.biomedcentral.com/1471-2172/12/56 kostenfrei https://doaj.org/toc/1471-2172 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2011 1, p 56 |
allfieldsGer |
10.1186/1471-2172-12-56 doi (DE-627)DOAJ033675716 (DE-599)DOAJ4e39400ea15a445bb664d5c1e75a985e DE-627 ger DE-627 rakwb eng RC581-607 Nawroth Peter P verfasserin aut RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The receptor for advanced glycation endproducts, RAGE, is involved in the pathogenesis of many inflammatory conditions, which is mostly related to its strong activation of NF-κB but also due to its function as ligand for the β<sub<2</sub<-integrin Mac-1. To further dissect the stimulus-dependent role of RAGE on leukocyte recruitment during inflammation, we investigated β<sub<2</sub<-integrin-dependent leukocyte adhesion in <it<RAGE<sup<-/- </sup<</it<and <it<Icam1<sup<-/- </sup<</it<mice in different cremaster muscle models of inflammation using intravital microscopy.</p< <p<Results</p< <p<We demonstrate that RAGE, but not ICAM-1 substantially contributes to N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced leukocyte adhesion in TNF-α-pretreated cremaster muscle venules in a Mac-1-dependent manner. In contrast, fMLP-stimulated leukocyte adhesion in unstimulated cremaster muscle venules is independent of RAGE, but dependent on ICAM-1 and its interaction with LFA-1. Furthermore, chemokine CXCL1-stimulated leukocyte adhesion in surgically prepared cremaster muscle venules was independent of RAGE but strongly dependent on ICAM-1 and LFA-1 suggesting a differential and stimulus-dependent regulation of leukocyte adhesion during inflammation in vivo.</p< <p<Conclusion</p< <p<Our results demonstrate that RAGE and ICAM-1 differentially regulate leukocyte adhesion in vivo in a stimulus-dependent manner.</p< Immunologic diseases. Allergy Lange-Sperandio Baerbel verfasserin aut Tschada Raphaela verfasserin aut Zablotskaya Victoria verfasserin aut Buschmann Kirsten verfasserin aut Dannenberg Susanne verfasserin aut Kamphues Anna verfasserin aut Frommhold David verfasserin aut Poeschl Johannes verfasserin aut Bierhaus Angelika verfasserin aut Sperandio Markus verfasserin aut In BMC Immunology BMC, 2003 12(2011), 1, p 56 (DE-627)326644962 (DE-600)2041500-X 14712172 nnns volume:12 year:2011 number:1, p 56 https://doi.org/10.1186/1471-2172-12-56 kostenfrei https://doaj.org/article/4e39400ea15a445bb664d5c1e75a985e kostenfrei http://www.biomedcentral.com/1471-2172/12/56 kostenfrei https://doaj.org/toc/1471-2172 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2011 1, p 56 |
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10.1186/1471-2172-12-56 doi (DE-627)DOAJ033675716 (DE-599)DOAJ4e39400ea15a445bb664d5c1e75a985e DE-627 ger DE-627 rakwb eng RC581-607 Nawroth Peter P verfasserin aut RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The receptor for advanced glycation endproducts, RAGE, is involved in the pathogenesis of many inflammatory conditions, which is mostly related to its strong activation of NF-κB but also due to its function as ligand for the β<sub<2</sub<-integrin Mac-1. To further dissect the stimulus-dependent role of RAGE on leukocyte recruitment during inflammation, we investigated β<sub<2</sub<-integrin-dependent leukocyte adhesion in <it<RAGE<sup<-/- </sup<</it<and <it<Icam1<sup<-/- </sup<</it<mice in different cremaster muscle models of inflammation using intravital microscopy.</p< <p<Results</p< <p<We demonstrate that RAGE, but not ICAM-1 substantially contributes to N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced leukocyte adhesion in TNF-α-pretreated cremaster muscle venules in a Mac-1-dependent manner. In contrast, fMLP-stimulated leukocyte adhesion in unstimulated cremaster muscle venules is independent of RAGE, but dependent on ICAM-1 and its interaction with LFA-1. Furthermore, chemokine CXCL1-stimulated leukocyte adhesion in surgically prepared cremaster muscle venules was independent of RAGE but strongly dependent on ICAM-1 and LFA-1 suggesting a differential and stimulus-dependent regulation of leukocyte adhesion during inflammation in vivo.</p< <p<Conclusion</p< <p<Our results demonstrate that RAGE and ICAM-1 differentially regulate leukocyte adhesion in vivo in a stimulus-dependent manner.</p< Immunologic diseases. Allergy Lange-Sperandio Baerbel verfasserin aut Tschada Raphaela verfasserin aut Zablotskaya Victoria verfasserin aut Buschmann Kirsten verfasserin aut Dannenberg Susanne verfasserin aut Kamphues Anna verfasserin aut Frommhold David verfasserin aut Poeschl Johannes verfasserin aut Bierhaus Angelika verfasserin aut Sperandio Markus verfasserin aut In BMC Immunology BMC, 2003 12(2011), 1, p 56 (DE-627)326644962 (DE-600)2041500-X 14712172 nnns volume:12 year:2011 number:1, p 56 https://doi.org/10.1186/1471-2172-12-56 kostenfrei https://doaj.org/article/4e39400ea15a445bb664d5c1e75a985e kostenfrei http://www.biomedcentral.com/1471-2172/12/56 kostenfrei https://doaj.org/toc/1471-2172 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2011 1, p 56 |
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RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner |
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RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner |
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Nawroth Peter P |
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BMC Immunology |
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BMC Immunology |
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Nawroth Peter P Lange-Sperandio Baerbel Tschada Raphaela Zablotskaya Victoria Buschmann Kirsten Dannenberg Susanne Kamphues Anna Frommhold David Poeschl Johannes Bierhaus Angelika Sperandio Markus |
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10.1186/1471-2172-12-56 |
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title_sort |
rage and icam-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner |
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RC581-607 |
title_auth |
RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner |
abstract |
<p<Abstract</p< <p<Background</p< <p<The receptor for advanced glycation endproducts, RAGE, is involved in the pathogenesis of many inflammatory conditions, which is mostly related to its strong activation of NF-κB but also due to its function as ligand for the β<sub<2</sub<-integrin Mac-1. To further dissect the stimulus-dependent role of RAGE on leukocyte recruitment during inflammation, we investigated β<sub<2</sub<-integrin-dependent leukocyte adhesion in <it<RAGE<sup<-/- </sup<</it<and <it<Icam1<sup<-/- </sup<</it<mice in different cremaster muscle models of inflammation using intravital microscopy.</p< <p<Results</p< <p<We demonstrate that RAGE, but not ICAM-1 substantially contributes to N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced leukocyte adhesion in TNF-α-pretreated cremaster muscle venules in a Mac-1-dependent manner. In contrast, fMLP-stimulated leukocyte adhesion in unstimulated cremaster muscle venules is independent of RAGE, but dependent on ICAM-1 and its interaction with LFA-1. Furthermore, chemokine CXCL1-stimulated leukocyte adhesion in surgically prepared cremaster muscle venules was independent of RAGE but strongly dependent on ICAM-1 and LFA-1 suggesting a differential and stimulus-dependent regulation of leukocyte adhesion during inflammation in vivo.</p< <p<Conclusion</p< <p<Our results demonstrate that RAGE and ICAM-1 differentially regulate leukocyte adhesion in vivo in a stimulus-dependent manner.</p< |
abstractGer |
<p<Abstract</p< <p<Background</p< <p<The receptor for advanced glycation endproducts, RAGE, is involved in the pathogenesis of many inflammatory conditions, which is mostly related to its strong activation of NF-κB but also due to its function as ligand for the β<sub<2</sub<-integrin Mac-1. To further dissect the stimulus-dependent role of RAGE on leukocyte recruitment during inflammation, we investigated β<sub<2</sub<-integrin-dependent leukocyte adhesion in <it<RAGE<sup<-/- </sup<</it<and <it<Icam1<sup<-/- </sup<</it<mice in different cremaster muscle models of inflammation using intravital microscopy.</p< <p<Results</p< <p<We demonstrate that RAGE, but not ICAM-1 substantially contributes to N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced leukocyte adhesion in TNF-α-pretreated cremaster muscle venules in a Mac-1-dependent manner. In contrast, fMLP-stimulated leukocyte adhesion in unstimulated cremaster muscle venules is independent of RAGE, but dependent on ICAM-1 and its interaction with LFA-1. Furthermore, chemokine CXCL1-stimulated leukocyte adhesion in surgically prepared cremaster muscle venules was independent of RAGE but strongly dependent on ICAM-1 and LFA-1 suggesting a differential and stimulus-dependent regulation of leukocyte adhesion during inflammation in vivo.</p< <p<Conclusion</p< <p<Our results demonstrate that RAGE and ICAM-1 differentially regulate leukocyte adhesion in vivo in a stimulus-dependent manner.</p< |
abstract_unstemmed |
<p<Abstract</p< <p<Background</p< <p<The receptor for advanced glycation endproducts, RAGE, is involved in the pathogenesis of many inflammatory conditions, which is mostly related to its strong activation of NF-κB but also due to its function as ligand for the β<sub<2</sub<-integrin Mac-1. To further dissect the stimulus-dependent role of RAGE on leukocyte recruitment during inflammation, we investigated β<sub<2</sub<-integrin-dependent leukocyte adhesion in <it<RAGE<sup<-/- </sup<</it<and <it<Icam1<sup<-/- </sup<</it<mice in different cremaster muscle models of inflammation using intravital microscopy.</p< <p<Results</p< <p<We demonstrate that RAGE, but not ICAM-1 substantially contributes to N-formyl-methionyl-leucyl-phenylalanine (fMLP)-induced leukocyte adhesion in TNF-α-pretreated cremaster muscle venules in a Mac-1-dependent manner. In contrast, fMLP-stimulated leukocyte adhesion in unstimulated cremaster muscle venules is independent of RAGE, but dependent on ICAM-1 and its interaction with LFA-1. Furthermore, chemokine CXCL1-stimulated leukocyte adhesion in surgically prepared cremaster muscle venules was independent of RAGE but strongly dependent on ICAM-1 and LFA-1 suggesting a differential and stimulus-dependent regulation of leukocyte adhesion during inflammation in vivo.</p< <p<Conclusion</p< <p<Our results demonstrate that RAGE and ICAM-1 differentially regulate leukocyte adhesion in vivo in a stimulus-dependent manner.</p< |
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title_short |
RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner |
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https://doi.org/10.1186/1471-2172-12-56 https://doaj.org/article/4e39400ea15a445bb664d5c1e75a985e http://www.biomedcentral.com/1471-2172/12/56 https://doaj.org/toc/1471-2172 |
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Lange-Sperandio Baerbel Tschada Raphaela Zablotskaya Victoria Buschmann Kirsten Dannenberg Susanne Kamphues Anna Frommhold David Poeschl Johannes Bierhaus Angelika Sperandio Markus |
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