Recruitment of classical monocytes can be inhibited by disturbing heteromers of neutrophil HNP1 and platelet CCL5

被引：116

作者：

Alard, Jean-Eric ^{[1
]}

Ortega-Gomez, Almudena ^{[1
]}

Wichapong, Kanin ^{[2
]}

Bongiovanni, Dario ^{[3
]}

Horckmans, Michael ^{[1
]}

Megens, Remco T. A. ^{[1
,2
]}

Leoni, Giovanna ^{[1
]}

Ferraro, Bartolo ^{[1
,4
]}

Rossaint, Jan ^{[5
]}

Paulin, Nicole ^{[1
]}

Ng, Judy ^{[3
]}

Ippel, Hans ^{[2
]}

Suylen, Dennis ^{[2
]}

Hinkel, Rabea ^{[1
,3
,6
]}

Blanchet, Xavier ^{[1
]}

Gaillard, Fanny ^{[7
]}

D'Amico, Michele ^{[4
]}

von Hundelshausen, Phillipp ^{[1
]}

Zarbock, Alexander ^{[5
]}

Scheiermann, Christoph ^{[8
]}

Hackeng, Tilman M. ^{[2
]}

Steffens, Sabine ^{[1
,6
]}

Kupatt, Christian ^{[3
,6
]}

Nicolaes, Gerry A. F. ^{[2
]}

Weber, Christian ^{[1
,2
,6
]}

Soehnlein, Oliver ^{[1
,6
,9
]}

机构：

[1] Univ Munich, Inst Cardiovasc Prevent, D-80336 Munich, Germany

[2] Univ Maastricht, Cardiovasc Res Inst Maastricht, Dept Biochem, NL-6200 Maastricht, Netherlands

[3] Tech Univ Munich, Med Klin 1, D-81675 Munich, Germany

[4] Univ Naples Federico II, Dept Expt Med, I-80138 Naples, Italy

[5] Univ Munster, Dept Anesthesiol, D-48149 Munster, Germany

[6] Munich Heart Alliance, German Ctr Cardiovasc Res, D-80336 Munich, Germany

[7] Univ Paris 06, Roscoff Biol Stn, F-29682 Paris, France

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

[9] Acad Med Ctr, Dept Pathol, NL-1105 Amsterdam, Netherlands

来源：

SCIENCE TRANSLATIONAL MEDICINE | 2015年 / 7卷 / 317期

基金：

欧洲研究理事会;

关键词：

INFLAMED ENDOTHELIUM; CHEMOKINE RECEPTORS; GRANULE DEFICIENCY; MONONUCLEAR-CELLS; FLOW CONDITIONS; ARREST; RANTES; BLOOD; CCR5; ATHEROSCLEROSIS;

D O I：

10.1126/scitranslmed.aad5330

中图分类号：

Q2 [细胞生物学];

学科分类号：

071013 [干细胞生物学];

摘要：

In acute and chronic inflammation, neutrophils and platelets, both of which promote monocyte recruitment, are often activated simultaneously. We investigated how secretory products of neutrophils and platelets synergize to enhance the recruitment of monocytes. We found that neutrophil-borne human neutrophil peptide 1 (HNP1, a-defensin) and platelet-derived CCL5 form heteromers. These heteromers stimulate monocyte adhesion through CCR5 ligation. We further determined structural features of HNP1-CCL5 heteromers and designed a stable peptide that could disturb proinflammatory HNP1-CCL5 interactions. This peptide attenuated monocyte and macrophage recruitment in a mouse model of myocardial infarction. These results establish the in vivo relevance of heteromers formed between proteins released from neutrophils and platelets and show the potential of targeting heteromer formation to resolve acute or chronic inflammation.

引用

页数：10

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