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December 2015


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Recruitment of classical monocytes can be inhibited by disturbing heteromers of neutrophil HNP1 and platelet CCL5, Science Translational Medicine 09 Dec 2015: DOI: 10.1126/scitranslmed.aad5330, DZHK authors: Bongiovanni, Horckmans, Paulin, Ng, Hinkel, von Hundelshausen, Steffens, Kupatt, Weber, Soehnlein

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DZHK investigators at the Munich partner site have succeeded in stopping monocyte accumulation at a site of inflammation. Their findings have been published in Science Translational Medicine. Monocytes play a vital role in the body’s immune system. But they can also pose a threat to the body when they accumulate in large numbers on the inner walls of blood vessels or in the heart muscle, where they can trigger inflammation or prevent healing. The research team, led by Oliver Söhnlein from the Institute for Cardiovascular Prevention (IPEK) at LMU Munich, developed a peptide in the laboratory which disrupts a key chemical signaling pathway: it prevents the most common type of white blood cell (neutrophils) and platelets from forming common docking sites for monocytes. Without these docking sites the monocytes cannot adhere to the vessel wall and inflammation does not develop. In this latest study, the team investigated the interaction between neutrophils and platelets in myocardial infarction, but the mechanism plays a relevant role whenever neutrophils and platelets are activated simultaneously. Consequently, the peptide could potentially be used as a basis for therapeutic intervention not only for acute myocardial infarction but also for chronic inflammation of the arteries or atherosclerosis. Oliver Söhnlein has already filed a patent application for the inhibitor peptide.

Link to the Paper