| Literature DB >> 29195076 |
Florian Gaertner1, Zerkah Ahmad2, Gerhild Rosenberger2, Shuxia Fan2, Leo Nicolai2, Benjamin Busch3, Gökce Yavuz2, Manja Luckner4, Hellen Ishikawa-Ankerhold2, Roman Hennel5, Alexandre Benechet6, Michael Lorenz2, Sue Chandraratne2, Irene Schubert2, Sebastian Helmer2, Bianca Striednig2, Konstantin Stark7, Marek Janko8, Ralph T Böttcher9, Admar Verschoor10, Catherine Leon11, Christian Gachet11, Thomas Gudermann12, Michael Mederos Y Schnitzler12, Zachary Pincus13, Matteo Iannacone6, Rainer Haas14, Gerhard Wanner4, Kirsten Lauber5, Michael Sixt15, Steffen Massberg16.
Abstract
Blood platelets are critical for hemostasis and thrombosis and play diverse roles during immune responses. Despite these versatile tasks in mammalian biology, their skills on a cellular level are deemed limited, mainly consisting in rolling, adhesion, and aggregate formation. Here, we identify an unappreciated asset of platelets and show that adherent platelets use adhesion receptors to mechanically probe the adhesive substrate in their local microenvironment. When actomyosin-dependent traction forces overcome substrate resistance, platelets migrate and pile up the adhesive substrate together with any bound particulate material. They use this ability to act as cellular scavengers, scanning the vascular surface for potential invaders and collecting deposited bacteria. Microbe collection by migrating platelets boosts the activity of professional phagocytes, exacerbating inflammatory tissue injury in sepsis. This assigns platelets a central role in innate immune responses and identifies them as potential targets to dampen inflammatory tissue damage in clinical scenarios of severe systemic infection.Entities:
Keywords: NETosis; cell migration; host-defense; innate immunity; mechanosensing; methicillin-resistant S. aureus; neutrophils; platelets; polarization; sepsis
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Year: 2017 PMID: 29195076 DOI: 10.1016/j.cell.2017.11.001
Source DB: PubMed Journal: Cell ISSN: 0092-8674 Impact factor: 41.582