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Atherosclerosis is characterized by the formation of atheromatous plaques which clog arteries. Microbiota plays a role in this disease, particularly in plaque formation and rupture.

Atherosclerosis starts with the deposit of fatty streaks in the arteries, on the surface of the intima, before true atheromatous plaques begin to form: these contain a lipid-rich core covered with a fibrous collagen-rich cap, aggregated platelets, and immune cells. A cascade of inflammatory reactions encourages plaque formation. The result is an obstruction of the arteries, which can prevent blood from reaching the organs and lead to infarction. Sometimes the plaque ruptures and causes cardiovascular problems. This process is responsible for 80% of sudden deaths (by stroke or myocardial infarction).1

Bacteria at fault?

The origin of plaque instability has not been determined, but it could be related to intestinal microbiota. Components produced by intestinal bacteria are suspected to be absorbed and then transported before finally being aggregated into the fatty streak.2 Bacteria may also be directly involved by infiltrating the atheromatous plaque and causing local inflammation.3 Bacteria observed in periodontitis have even been observed in atheromatous plaques, suggesting their role in plaque formation and even rupture.4 Other disease risk factors have been observed, particularly hypercholesterolemia and smoking, as well as dysbiosis associated with a high fat diet.5 The hypothesis of the connection between bacteria present in the plaque and an elevated concentration of cholesterol is linked to the role of the metabolite TMAO (trimethylamine N-oxide), produced by the intestinal microbiota from dietary choline (eggs, meat), which has an inflammatory action.5,6

Work on microbiota

These observations make it possible to consider prevention via diet – the Mediterranean diet has been proven effective7 – but also by working on the equilibrium in microbiota in connection with lipid balance, in order to control the development of atheromatous plaques. In this regard, diets rich in fish oil (omega 3), dietary fiber, polyphenol, or with probiotic supplements may impact the cardiovascular risk.8-9 Their anti-inflammatory properties, action on the intestinal barrier, and stimulation of bacteria that produce volatile short-chain fatty acids are assets in preventing atherosclerosis.9-11


1. (consulté le 20/04/2017)
2. Tang WH et al. Intestinal microbialmetabolism of phosphatidylcholine and cardiovascular risk. N Engl J Med 2013 ; 368 : 1575-84.
3. Koren O et al. Human oral, gut, and plaque microbiota in patients with atherosclerosis. PNAS 2011 ; 108 : 4592-8.
4. Zelkha SA et al. Periodontal innate immune mechanisms relevant to atherosclerosis and obesity. Periodontology 2000 2010 ; 54 : 207-21.
5. Wang Z et al. Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature 2011 ; 472 : 57-63.
6.Wang Z et al., Non-lethal Inhibition of Gut Microbial Trimethylamine Production
for the Treatment of Atherosclerosis. Cell 2015 ; 163, 1585–1595
7. Estruch R et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med 2013; 368: 1279-90.
8. Yu HN et al. Effects of fish oil with a high content of n-3 polyunsaturated fatty acids on mouse gut microbiota. Arch Med Res 2014 ; 45 : 195-202.
9. Fava F, Lovegrove JA, Gitau R, Jackson KG, Tuohy KM. The gut microbiota and lipid metabolism: implications for human health and coronary heart disease. Curr Med Chem2006 ; 13 : 3005-21.
10 Wong JM. Gut microbiota and cardiometabolic outcomes: influence of dietary patterns and their associated components. Am J Clin Nutr 2014 ; 100 : 369S-77S
11 Jonsson AL, Bäckhed F. Role of gut microbiota in atherosclerosis. Nat Rev Cardiol. 2017 Feb;14(2):79-87. doi: 10.1038/nrcardio.2016.183. Epub 2016 Dec 1. Review. PubMed PMID: 27905479.

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The Biocodex Microbiota Institute: an international leader in microbiota