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The Commensal Microbiota Enhances ADP-Triggered Integrin αIIbβ3 Activation and von Willebrand Factor-Mediated Platelet Deposition to Type I Collagen

1
Center for Thrombosis and Hemostasis (CTH), University Medical Center of the Johannes Gutenberg- University of Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany
2
German Center for Cardiovascular Research (DZHK), Partner Site RheinMain, 55131 Mainz, Germany
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2020, 21(19), 7171; https://doi.org/10.3390/ijms21197171
Received: 29 August 2020 / Revised: 21 September 2020 / Accepted: 25 September 2020 / Published: 28 September 2020
(This article belongs to the Special Issue Molecular Research on Arteriosclerosis and Thrombosis)
The commensal microbiota is a recognized enhancer of arterial thrombus growth. While several studies have demonstrated the prothrombotic role of the gut microbiota, the molecular mechanisms promoting arterial thrombus growth are still under debate. Here, we demonstrate that germ-free (GF) mice, which from birth lack colonization with a gut microbiota, show diminished static deposition of washed platelets to type I collagen compared with their conventionally raised (CONV-R) counterparts. Flow cytometry experiments revealed that platelets from GF mice show diminished activation of the integrin αIIbβ3 (glycoprotein IIbIIIa) when activated by the platelet agonist adenosine diphosphate (ADP). Furthermore, washed platelets from Toll-like receptor-2 (Tlr2)-deficient mice likewise showed impaired static deposition to the subendothelial matrix component type I collagen compared with wild-type (WT) controls, a process that was unaffected by GPIbα-blockade but influenced by von Willebrand factor (VWF) plasma levels. Collectively, our results indicate that microbiota-triggered steady-state activation of innate immune pathways via TLR2 enhances platelet deposition to subendothelial matrix molecules. Our results link host colonization status with the ADP-triggered activation of integrin αIIbβ3, a pathway promoting platelet deposition to the growing thrombus. View Full-Text
Keywords: microbiota; germ-free; von Willebrand factor; Toll-like receptor-2; platelets; αIIbβ3 microbiota; germ-free; von Willebrand factor; Toll-like receptor-2; platelets; αIIbβ3
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MDPI and ACS Style

Kiouptsi, K.; Jäckel, S.; Wilms, E.; Pontarollo, G.; Winterstein, J.; Karwot, C.; Groß, K.; Jurk, K.; Reinhardt, C. The Commensal Microbiota Enhances ADP-Triggered Integrin αIIbβ3 Activation and von Willebrand Factor-Mediated Platelet Deposition to Type I Collagen. Int. J. Mol. Sci. 2020, 21, 7171. https://doi.org/10.3390/ijms21197171

AMA Style

Kiouptsi K, Jäckel S, Wilms E, Pontarollo G, Winterstein J, Karwot C, Groß K, Jurk K, Reinhardt C. The Commensal Microbiota Enhances ADP-Triggered Integrin αIIbβ3 Activation and von Willebrand Factor-Mediated Platelet Deposition to Type I Collagen. International Journal of Molecular Sciences. 2020; 21(19):7171. https://doi.org/10.3390/ijms21197171

Chicago/Turabian Style

Kiouptsi, Klytaimnistra; Jäckel, Sven; Wilms, Eivor; Pontarollo, Giulia; Winterstein, Jana; Karwot, Cornelia; Groß, Kathrin; Jurk, Kerstin; Reinhardt, Christoph. 2020. "The Commensal Microbiota Enhances ADP-Triggered Integrin αIIbβ3 Activation and von Willebrand Factor-Mediated Platelet Deposition to Type I Collagen" Int. J. Mol. Sci. 21, no. 19: 7171. https://doi.org/10.3390/ijms21197171

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