Helicobacter Pylori Infection Induces Intestinal Dysbiosis That Could Be Related to the Onset of Atherosclerosis

Abstract

Cardiovascular diseases represent one of the first causes of death around the world, and atherosclerosis is one of the first steps in the development of them. Although these problems occur mainly in elderly, the incidence in younger people is being reported, and an undetermined portion of patients without the classic risk factors develop subclinical atherosclerosis at earlier stages of life. Recently, both the H. pylori infection and the intestinal microbiota have been linked to atherosclerosis. The mechanisms behind those associations are poorly understood, but some of the proposed explanations are (a) the effect of the chronic systemic inflammation induced by H. pylori, (b) a direct action over the endothelial cells by the cytotoxin associated gene A protein, and (c) alterations of the lipid metabolism and endothelial dysfunction induced by H. pylori infection. Regarding the microbiota, several studies show that induction of atherosclerosis is related to high levels of Trimethylamine N-oxide. In this review, we present the information published about the effects of H. pylori over the intestinal microbiota and their relationship with atherosclerosis and propose a hypothesis to explain the nature of these associations. If H. pylori contributes to atherosclerosis, then interventions for eradication and restoration of the gut microbiota at early stages could represent a way to prevent disease progression.

Re-evaluation of dietary interventions in rheumatoid arthritis: can we improve patient conversations around food choices?

“…Cigarette smoke, a common synthetic toxin, is known to create dysbiosis [ 96 ] and increase risk of RA [ 97 ]. In other individuals, Helicobacter pylori ( H. pylori ) infection can drive dysbiosis [ 98 ] and increase risk of developing RA, particularly in women under the age of 30 [ 99 ]. Importantly, H. pylori treatment has been shown to significantly reduce inflammatory markers and improve clinical outcome measures [ 100 ].…”

The Interplay between Helicobacter pylori and Gut Microbiota in Non-Gastrointestinal Disorders: A Special Focus on Atherosclerosis

“…Specifically, H. pylori infection modulates the production of gastrokine (GKN)-1, a protein involved in mucosal repair and healing. Patients infected with H. pylori have lower levels of GKN-1, which may not only impair intestinal mucosal healing and promote the development of leaky gut, but also directly affect intestinal eubiosis [96]. Interestingly, the effects of H. pylori seem to mainly involve Firmicutes that can produce TMA and TMAO, which are associated with endothelial dysfunction and atherosclerosis [97].…”

Helicobacter cinaedi bacterium association with atherosclerosis and other diseases

“…The chronic inflammatory process induced by the bacterium is thought to be an indirect mechanism of endothelial cell damage contributing to the development of atherosclerosis ( Chmiela et al, 2015 ; Krupa et al, 2021 ). Another hypothesis suggests that the interaction of H. pylori with other members of the internal microflora may lead to dysbiosis, resulting in increased levels of trimethylamine N-oxide, which is an inducer of endothelial damage, in serum ( Francisco, 2022 ). Therefore, the role of microflora (including bacteria associated with atherosclerotic plaques) in the development of atherosclerosis is still not fully understood.…”