Role of gut microbiota in the modulation of atherosclerosis-associated immune response.

Inflammation and metabolic abnormalities are linked to each other. At present, pathogenic inflammatory response was recognized as a major player in metabolic diseases. In humans, intestinal microflora could significantly influence the development of metabolic diseases including atherosclerosis.

Intestinal mucosal tolerance and impact of gut microbiota to mucosal tolerance.

The mucosal barriers are very sensitive to pathogenic infection, thereby assuming the capacity of the mucosal immune system to induce protective immunity to harmful antigens and tolerance against harmless substances. This review provides current information about mechanisms of induction of mucosal tolerance and about impact of gut microbiota to mucosal tolerance.

Infection-associated biomarkers of inflammation in atherosclerosis.

Atherosclerosis is a systemic inflammatory disease leading to lipid-laden inflammatory lesions in the arterial walls that may destabilize and rupture. It is becoming clear that addressing the "classical" risk factors for atherosclerosis does not entirely reduce the risk of cardiovascular events. Novel biomarkers to be used in highthroughput assays are necessary for diagnosis, for determination of the residual risk and for monitoring the effects of the therapy.

View of statins as antimicrobials in cardiovascular risk modification.

Atherosclerosis is a complex arterial pathological development underlying heart attack and stroke and a leading cause of death in developed and now also in developing countries. The primary processes that lead to the inflammatory lipid-laden proliferative lesion, obstructing the blood flow, and referred to as atherosclerotic plaque are dyslipidaemia and inflammation. Here, we will review one of the most efficient classes of drugs indicated for management of cardiovascular disease (CVD), statins.

Periodontal bacterial invasion and infection: contribution to atherosclerotic pathology.

Objective: The objective of this review was to perform a systematic evaluation of the literature reporting current scientific evidence for periodontal bacteria as contributors to atherosclerosis.

Methods: Literature from epidemiological, clinical and experimental studies concerning periodontal bacteria and atherosclerosis were reviewed. Gathered data were categorized into seven "proofs" of evidence that periodontal bacteria: 1) disseminate from the oral cavity and reach systemic vascular tissues; 2) can be found in the affected tissues; 3) live within the affected site; 4) invade affected cell types in vitro; 5) induce atherosclerosis in animal models of disease; 6) non-invasive mutants of periodontal bacteria cause significantly reduced pathology in vitro and in vivo; and 7) periodontal isolates from human atheromas can cause disease in animal models of infection.