Sialyltransferase ST3Gal-IV controls CXCR2-mediated firm leukocyte arrest during inflammation

被引：67

作者：

Frommhold, David ^{[13
]}

Ludwig, Andreas ^{[2
]}

Bixel, M. Gabriele ^{[3
]}

Zarbock, Alexander ^{[4
,10
]}

Babushkina, Inna ^{[13
]}

Weissinger, Melitta ^{[13
]}

Cauwenberghs, Sandra ^{[2
]}

Ellies, Lesley G. ^{[5
]}

Marth, Jamey D. ^{[6
,7
]}

Beck-Sickinger, Annette G. ^{[8
]}

Sixt, Michael ^{[9
]}

Lange-Sperandio, Baerbel ^{[11
]}

Zernecke, Alma ^{[2
]}

Brandt, Ernst ^{[12
]}

Weber, Christian ^{[2
]}

Vestweber, Dietmar ^{[3
]}

Ley, Klaus ^{[4
]}

Sperandio, Markus ^{[1
]}

机构：

[1] Univ Munich, Walter Brendel Ctr Expt Med, D-81377 Munich, Germany

[2] Rhein Westfal TH Aachen, Inst Mol Cardiovasc Res, D-52074 Aachen, Germany

[3] Max Planck Inst Mol Biomed, D-48149 Munster, Germany

[4] La Jolla Inst Allergy & Immunol, La Jolla, CA 92037 USA

[5] Univ Calif San Diego, Dept Pathol, La Jolla, CA 92093 USA

[6] Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA

[7] Univ Calif San Diego, Howard Hughes Med Inst, La Jolla, CA 92093 USA

[8] Univ Leipzig, Inst Biochem, D-04103 Leipzig, Germany

[9] Max Planck Inst Biochem, D-82152 Martinsried, Germany

[10] Univ Munster, Dept Anesthesiol & Crit Care Med, D-48149 Munster, Germany

[11] Univ Munich, Dr v Haunersches Childrens Hosp, D-80336 Munich, Germany

[12] Res Ctr Borstel, D-23845 Borstel, Germany

[13] Univ Heidelberg, Childrens Hosp, D-69120 Heidelberg, Germany

来源：

JOURNAL OF EXPERIMENTAL MEDICINE | 2008年 / 205卷 / 06期

关键词：

D O I：

10.1084/jem.20070846

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Recent in vitro studies have suggested a role for sialylation in chemokine receptor binding to its ligand (Bannert, N., S. Craig, M. Farzan, D. Sogah, N. V. Santo, H. Choe, and J. Sodroski. 2001. J. Exp. Med. 194: 1661-1673). This prompted us to investigate chemokine-induced leukocyte adhesion in inflamed cremaster muscle venules of alpha 2,3 sialyltransferase (ST3Gal-IV)-deficient mice. We found a marked reduction in leukocyte adhesion to inflamed microvessels upon injection of the CXCR2 ligands CXCL1 (keratinocyte-derived chemokine) or CXCL8 (interleukin 8). In addition, extravasation of ST3Gal-IV-/- neutrophils into thioglycollate-pretreated peritoneal cavities was significantly decreased. In vitro assays revealed that CXCL8 binding to isolated ST3Gal-IV-/- neutrophils was markedly impaired. Furthermore, CXCL1-mediated adhesion of ST3Gal-IV-/- leukocytes at physiological flow conditions, as well as transendothelial migration of ST3Gal-IV-/- leukocytes in response to CXCL1, was significantly reduced. In human neutrophils, enzymatic desialylation decreased binding of CXCR2 ligands to the neutrophil surface and diminished neutrophil degranulation in response to these chemokines. In addition, binding of alpha 2,3-linked sialic acid-specific Maackia amurensis lectin II to purified CXCR2 from neuraminidase-treated CXCR2-transfected HEK293 cells was markedly impaired. Collectively, we provide substantial evidence that sialylation by ST3Gal-IV significantly contributes to CXCR2-mediated leukocyte adhesion during inflammation in vivo.

引用

页码：1435 / 1446

页数：12

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