Editors' ChoiceImmunology

Anti-inflammatory strategies reach for the SKY

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Science Signaling  15 Dec 2015:
Vol. 8, Issue 407, pp. ec372
DOI: 10.1126/scisignal.aae0547

Inflammation aids the body’s response to infection or injury but can cause damage if excessive or unresolved. Alard et al. examined how two early inflammatory mediators—neutrophils and platelets—cooperate to enhance inflammation. They found that human neutrophil peptide 1 (HNP1), which is secreted from neutrophils, forms a heteromer with the chemokine CCL5 on platelets, resulting in enhanced monocyte adhesion and an increase in inflammation. Disrupting this interaction with a peptide (SKY) decreased inflammation and blocked monocyte recruitment in a mouse model of myocardial infarction. If these results hold true in humans, they could form the basis for a new specific therapeutic in inflammation-associated diseases.

J.-E. Alard, A. Ortega-Gomez, K. Wichapong, D. Bongiovanni, M. Horckmans, R. T. A. Megens, G. Leoni, B. Ferraro, J. Rossaint, N. Paulin, J. Ng, H. Ippel, D. Suylen, R. Hinkel, X. Blanchet, F. Gaillard, M. D’Amico, P. von Hundelshausen, A. Zarbock, C. Scheiermann, T. M. Hackeng, S. Steffens, C. Kupatt, G. A. F. Nicolaes, C. Weber, O. Soehnlein, Recruitment of classical monocytes can be inhibited by disturbing heteromers of neutrophil HNP1 and platelet CCL5. Sci. Transl. Med. 7, 317ra196 (2015). [Abstract]

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