The Effects of Probiotics on Inflammation, Endothelial Dysfunction, and Atherosclerosis Progression: A Mechanistic Overview.

INTRODUCTION

The relationship between the intestinal microbiota dysbiosis, inflammation, and cardiovascular disorders (CVDs) has become evident, based on a growing body of literature from animal models and human studies. On the other hand, probiotics are believed to have promising effects on modifying dysbiosis and protecting against CVDs.

OBJECTIVE

This narrative review provides an overview of the link between gut microbiota, inflammation, endothelial dysfunction, and atherosclerosis. The influences of probiotic supplementation on biomarkers contributing to these conditions as the primary underlying risk factors for developing CVDs are also discussed.

METHODS

An up-to-date review was performed of the available evidence from experimental studies, clinical trials, and meta-analyses, considering their challenges and limitations. It also aimed to provide mechanistic insight into the likely mechanisms of probiotics that could prevent atherosclerosis initiation and progression.

RESULTS

Probiotic supplementation seems to be associated with reduced levels of inflammation and oxidative stress biomarkers (C-reactive protein, tumour necrosis factor-α, interleukin (IL)-6, IL-12, and malondialdehyde). Further, these agents might enhance antioxidant factors (IL-10, total antioxidant status, total antioxidant capacity, glutathione, and nitric oxide). Probiotics also appear to improve intestinal barrier integrity, reduce leakage of harmful metabolites (e.g., lipopolysaccharides), inhibit pro-inflammatory signalling pathways, and possibly suppress the formation of trimethylamine/trimethylamine oxide. Probiotics have also been found to enhance endothelial function and halter thrombosis.

CONCLUSION

The current clinical evidence underlines belief that probiotics might be associated with reduced levels of inflammation biomarkers. Experimental evidence reports that the beneficial effects of probiotics seem to be mainly imposed by triggering the secretion of short-chain fatty acids and bile acids, in addition to suppressing the NF-κB signalling pathway. However, the current studies are still in their infancy and it is of high priority to design further research on the topic.