A novel pathway of HMGB1-mediated inflammatory cell recruitment that requires Mac-1-integrin

被引:312
作者
Orlova, Valeria V.
Choi, Eun Young
Xie, Changping
Chavakis, Emmanouil
Bierhaus, Angelika
Ihanus, Eveliina
Ballantyne, Christie M.
Gahmberg, Carl G.
Bianchi, Marco E.
Nawroth, Peter P.
Chavakis, Triantafyllos
机构
[1] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA
[2] Heidelberg Univ, Dept Internal Med 1, D-6900 Heidelberg, Germany
[3] Goethe Univ Frankfurt, Dept Internal Med 3, D-6000 Frankfurt, Germany
[4] Univ Helsinki, Fac Biosci, Div Biochem, FIN-00014 Helsinki, Finland
[5] Baylor Coll Med, Dept Med, Sect Atherosclerosis & Lipoprot Res, Houston, TX 77030 USA
[6] Methodist DeBakey Heart Ctr, Ctr Cardiovasc Dis Prevent, Houston, TX USA
[7] San Raffaele Univ, Fac Med, Milan, Italy
关键词
adhesion; inflammation; integrins; neutrophils;
D O I
10.1038/sj.emboj.7601552
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
High-mobility group box 1 (HMGB1) is released extra-cellularly upon cell necrosis acting as a mediator in tissue injury and inflammation. However, the molecular mechanisms for the proinflammatory effect of HMGB1 are poorly understood. Here, we define a novel function of HMGB1 in promoting Mac-1-dependent neutrophil recruitment. HMGB1 administration induced rapid neutrophil recruitment in vivo. HMGB1-mediated recruitment was prevented in mice deficient in the beta 2-integrin Mac-1 but not in those deficient in LFA-1. As observed by bone marrow chimera experiments, Mac-1-dependent neutrophil recruitment induced by HMGB1 required the presence of receptor for advanced glycation end products ( RAGE) on neutrophils but not on endothelial cells. In vitro, HMGB1 enhanced the interaction between Mac-1 and RAGE. Consistently, HMGB1 activated Mac-1 as well as Mac-1-mediated adhesive and migratory functions of neutrophils in a RAGE-dependent manner. Moreover, HMGB1-induced activation of nuclear factor-kappa B in neutrophils required both Mac-1 and RAGE. Together, a novel HMGB1-dependent pathway for inflammatory cell recruitment and activation that requires the functional interplay between Mac-1 and RAGE is described here.
引用
收藏
页码:1129 / 1139
页数:11
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