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.

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.

Klebsiella pneumoniae induces an inflammatory response in human retinal-pigmented epithelial cells.

Purpose: The retinal pigment epithelium (RPE) is a barrier to Klebsiella pneumoniae infection in endogenous endophthalmitis. Nevertheless, the inflammatory response of RPE cells upon interaction with this pathogen has not been studied. Here we tested the hypothesis that K.

Bacterial invasion of vascular cell types: vascular infectology and atherogenesis.

To portray the chronic inflammation in atherosclerosis, leukocytic cell types involved in the immune response to invading pathogens are often the focus. However, atherogenesis is a complex pathological deterioration of the arterial walls, where vascular cell types are participants with regards to deterioration and disease. Since other recent reviews have detailed the role of both the innate and adaptive immune response in atherosclerosis, herein we will summarize the latest developments regarding the association of bacteria with vascular cell types: infections as a risk factor for atherosclerosis; bacterial invasion of vascular cell types; the atherogenic sequelae of bacterial presence such as endothelial activation and blood clotting; and the identification of the species that are able to colonize this niche.

Both the unique and repeat regions of the Porphyromonas gingivalis hemagglutin A are involved in adhesion and invasion of host cells.

Porphyromonas gingivalis is one of the major etiologic agents of adult periodontitis and has been associated with cardiovascular diseases. It expresses multiple hemagglutinins that are significant virulence factors and play an important role in bacterial attachment and invasion of host cells. The objective of this study was to determine the impact of P.

Genomic comparison of invasive and rare non-invasive strains reveals Porphyromonas gingivalis genetic polymorphisms.

Background: Porphyromonas gingivalis strains are shown to invade human cells in vitro with different invasion efficiencies, varying by up to three orders of magnitude.

Objective: We tested the hypothesis that invasion-associated interstrain genomic polymorphisms are present in P. gingivalis and that putative invasion-associated genes can contribute to P.

Cultivation of Enterobacter hormaechei from human atherosclerotic tissue.

Aim: To determine whether culturable bacterial strains are present in human atheromatous tissue and to investigate their properties using culture, quantitative PCR, metagenomic screening, genomic and biochemical methods.

Methods: We analyzed femoral atherosclerotic plaque and five pairs of diseased and healthy arterial tissue for the presence of culturable bacteria using cell cultures and genomic analysis.

Results: Gram negative aerobic bacilli were cultivated from the plaque tissue.

Intracellular survival and vascular cell-to-cell transmission of Porphyromonas gingivalis.

Background: Porphyromonas gingivalis is associated with periodontal disease and invades different cell types including epithelial, endothelial and smooth muscle cells. In addition to P. gingivalis DNA, we have previously identified live invasive bacteria in atheromatous tissue.

Detection of bacterial DNA in atheromatous plaques by quantitative PCR.

This is the first study to analyze atheromatous plaques for the presence of bacterial DNA from ten species, including periodontal species and Chlamydia pneumoniae. We examined 129 samples of DNA extracted from atheromas from 29 individuals for the presence of bacterial 16S rDNA sequences from ten different species: Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans (A.a.

Hemagglutinin B is involved in the adherence of Porphyromonas gingivalis to human coronary artery endothelial cells.

Porphyromonas gingivalis is a periodontopathogen that may play a role in cardiovascular diseases. Hemagglutinins may function as adhesins and are required for virulence of several bacterial pathogens. The aim of this study was to determine the role of hemagglutinin B (HagB) in adherence of P.

Genes of periodontopathogens expressed during human disease.

Background: Since many bacterial genes are environmentally regulated, the screening for virulence-associated factors using classical genetic and molecular biology approaches can be biased under laboratory growth conditions of a given pathogen, because the required conditions for expression of many virulence factors may not occur during in vitro growth. Thus, technologies have been developed during the past several years to identify genes that are expressed during disease using animal models of human disease. However, animal models are not always truly representative of human disease, and with many pathogens, there is no appropriate animal model.