A holobiont view on thrombosis: unravelling the microbiota’s influence on arterial thrombus growth
Authors:Giulia Pontarollo1, Klytaimnistra Kiouptsi1 and Christoph Reinhardt1,2
doi: 10.15698/mic2020.01.704
Volume 7, pp. 28 to 31, published 06/01/2020.
1 Center for Thrombosis and Hemostasis (CTH), University Medical Center Mainz, Johannes Gutenberg University of Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
2 German Center for Cardiovascular Research (DZHK), Partner Site RheinMain, Mainz, Germany.
Keywords:
microbiota, germ-free, arterial thrombosis, atherothrombosis, carotid artery, atherosclerosis mouse models, late atherosclerosis, cholesterol, platelet
Corresponding Author(s):
Conflict of interest statement:
The authors declare no conflict of interests.
Please cite this article as:
Giulia Pontarollo, Klytaimnistra Kiouptsi and Christoph Reinhardt (2020). A holobiont view on thrombosis: unravelling the microbiota’s influence on arterial thrombus growth. Microbial Cell 7(1): 28-31. doi: 10.15698/mic2020.01.704
© 2020 Pontarollo et al. This is an open-access article released under the terms of the Crea-tive Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduction in any medium, provided the original author and source are acknowledged.
Abstract:
The commensal microbiota has co-evolved with its host, colonizing all body surfaces. Therefore, this microbial ecosystem is intertwined with host physiology at multiple levels. While it is evident that microbes that reach the blood stream can trigger thrombus formation, it remains poorly explored if the wealth of microbes that colonize the body surfaces of the mammalian host can be regarded as a modifier of cardiovascular disease (CVD) development. To experimentally address the microbiota’s role in the development of atherosclerotic lesions and arterial thrombosis, we generated a germ-free (GF) low-density lipoprotein receptor-deficient (Ldlr-/-) atherosclerosis mouse model (Kiouptsi et al., mBio, 2019) and explored the role of nutritional composition on arterial thrombogenesis.