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...
| Main Authors: | , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
BMC
2011-10-01
|
| Series: | BMC Immunology |
| Online Access: | http://www.biomedcentral.com/1471-2172/12/56 |
| _version_ | 1818054672277045248 |
|---|---|
| author | Nawroth Peter P Lange-Sperandio Baerbel Tschada Raphaela Zablotskaya Victoria Buschmann Kirsten Dannenberg Susanne Kamphues Anna Frommhold David Poeschl Johannes Bierhaus Angelika Sperandio Markus |
| author_facet | Nawroth Peter P Lange-Sperandio Baerbel Tschada Raphaela Zablotskaya Victoria Buschmann Kirsten Dannenberg Susanne Kamphues Anna Frommhold David Poeschl Johannes Bierhaus Angelika Sperandio Markus |
| author_sort | Nawroth Peter P |
| collection | DOAJ |
| description | <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> |
| first_indexed | 2024-12-10T12:00:46Z |
| format | Article |
| id | doaj.art-4e39400ea15a445bb664d5c1e75a985e |
| institution | Directory Open Access Journal |
| issn | 1471-2172 |
| language | English |
| last_indexed | 2024-12-10T12:00:46Z |
| publishDate | 2011-10-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Immunology |
| spelling | doaj.art-4e39400ea15a445bb664d5c1e75a985e2022-12-22T01:49:38ZengBMCBMC Immunology1471-21722011-10-011215610.1186/1471-2172-12-56RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent mannerNawroth Peter PLange-Sperandio BaerbelTschada RaphaelaZablotskaya VictoriaBuschmann KirstenDannenberg SusanneKamphues AnnaFrommhold DavidPoeschl JohannesBierhaus AngelikaSperandio Markus<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>http://www.biomedcentral.com/1471-2172/12/56 |
| spellingShingle | Nawroth Peter P Lange-Sperandio Baerbel Tschada Raphaela Zablotskaya Victoria Buschmann Kirsten Dannenberg Susanne Kamphues Anna Frommhold David Poeschl Johannes Bierhaus Angelika Sperandio Markus RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner BMC Immunology |
| title | RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner |
| title_full | RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner |
| title_fullStr | RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner |
| title_full_unstemmed | RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner |
| title_short | RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner |
| title_sort | rage and icam 1 differentially control leukocyte recruitment during acute inflammation in a stimulus dependent manner |
| url | http://www.biomedcentral.com/1471-2172/12/56 |
| work_keys_str_mv | AT nawrothpeterp rageandicam1differentiallycontrolleukocyterecruitmentduringacuteinflammationinastimulusdependentmanner AT langesperandiobaerbel rageandicam1differentiallycontrolleukocyterecruitmentduringacuteinflammationinastimulusdependentmanner AT tschadaraphaela rageandicam1differentiallycontrolleukocyterecruitmentduringacuteinflammationinastimulusdependentmanner AT zablotskayavictoria rageandicam1differentiallycontrolleukocyterecruitmentduringacuteinflammationinastimulusdependentmanner AT buschmannkirsten rageandicam1differentiallycontrolleukocyterecruitmentduringacuteinflammationinastimulusdependentmanner AT dannenbergsusanne rageandicam1differentiallycontrolleukocyterecruitmentduringacuteinflammationinastimulusdependentmanner AT kamphuesanna rageandicam1differentiallycontrolleukocyterecruitmentduringacuteinflammationinastimulusdependentmanner AT frommholddavid rageandicam1differentiallycontrolleukocyterecruitmentduringacuteinflammationinastimulusdependentmanner AT poeschljohannes rageandicam1differentiallycontrolleukocyterecruitmentduringacuteinflammationinastimulusdependentmanner AT bierhausangelika rageandicam1differentiallycontrolleukocyterecruitmentduringacuteinflammationinastimulusdependentmanner AT sperandiomarkus rageandicam1differentiallycontrolleukocyterecruitmentduringacuteinflammationinastimulusdependentmanner |