Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to assess the real significance of some plasma and vascular indices in disorders of the stable course of coronary heart disease (CHD) in chronic bacterial- and viral infection-invasion, we determined the blood plasma lipid hydrogen peroxide (LHP) activity, a direct index of the lipid peroxidation degree, and measured the concentration of specific antibodies to Chlamydia pneumoniae (C. pneunoniae), herpes simplex virus type 1 (HSV-1), cytomegalovirus (CMV) and Epstein-Barr virus (EBV) by means of the enzyme-linked immunosorbent assay (ELISA). We examined a total of 70 patients presenting with CHD combined with a concomitant infection both with a stable course of the disease (Group One) and acute coronary syndrome (Group Two), as well as 50 infected people without verified signs of coronary atherosclerosis (Group Three). The comparison group consisted of patients with CHD, being seronegative for the causative agents referred to above. The condition of the major vessels was appropriately assessed by means of duplex ultrasonography (DU). Resulting from the findings of the carried out investigation, we singled out a triad of symptoms characteristic of the transformation of the chronic infectious process into the recurrent phase, which for the CHD patients with the presence of the conventional risk factors of atherosclerosis might become a cause of the disordered stable course of the disease and development of acute ischaemic attacks. The revealed alterations seemed to have been based upon an infectious-origin inflammatory lesion of the vessels, which was duly confirmed by duplex ultrasonography.
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PMID:[Chronic bacterial-and-viral vasculitis as a possible risk factor of disordered stability of the coronary atherosclerosis course]. 1764 12

It is assumed that various infectious agents play direct or indirect roles in the pathogenesis of atherosclerosis which is accepted as a chronic inflammatory phenomenon. However, the data obtained from different studies are contradictory. The aim of this study was to investigate the roles of herpes virus group [Herpes simplex virus (HSV), Epstein-Barr virus (EBV), Cytomegalovirus (CMV)] and hepatitis A virus (HAV) which are debated in terms of their impact in the pathogenesis of coronary arterial diseases. For this purpose, atherome plaque samples collected from 28 patients (23 were male; age range: 43-74 years) with atherosclerotic heart disease and vein samples from 22 control patients (19 were male; age range: 37-85 years) who had vascular diseases other than atherosclerosis, were investigated by means of the presence of nucleic acids of the above mentioned viruses by real-time polymerase chain reaction (PCR). Besides, classical cardiovascular risk factors (hypertension, hyperlipidemia, hypercholestrolemia, diabetes mellitus, smoking habits, gender, age and familial background) were questioned in both patient and control groups. As a result, no positivity were detected for nucleic acids of HSV type 1 and 2, EBV and HAV, whereas CMV-DNA was found positive in three of 28 (10.7%) atheromateous plaques (viral loads were 21, 188 and 288 copies/mg). Amongst 22 vascular samples from controls, two (9.1%) yielded positive results for EBV-DNA (viral loads were 5 and 10 copies/mg), while the other samples were found negative for nucleic acids of HSV type 1 and 2, CMV and HAV. The evaluation of the known risk factors for atherosclerosis revealed that, the difference between the presence of hypertension and hyperlipidemia which are the major risk factors, was statistically important (p < 0.05) in patient group (64% and 50%, respectively) and control group (32% and 23%, respectively). In conclusion, the hypothesis concerning the possible relationship between these viral agents and the progression of atherosclerosis, have not been supported by our data which are similar to the results obtained from various other studies. Actually, further studies are needed to clarify such direct or indirect roles of infectious agents in the pathogenesis of coronary arterial diseases.
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PMID:[Investigation of herpes group and hepatitis A virus nucleic acids in the atherome plaque samples of patients with coronary arterial disease]. 1817 72

Atherosclerosis is characterized by a complex immune response in the vessel wall, involving both inflammation and autoimmune processes. Epstein-Barr virus-induced gene 3 (Ebi3) is a member of the interleukin (IL)-12 heterodimeric cytokine family, which has important immunomodulatory functions. To date, little is known about the role of Ebi3 in vascular disease. We examined the expression of Ebi3 in human atheromatous lesions and analyzed its transcriptional regulation in vascular cells. The in situ expression of Ebi3 in human endarterectomy specimens was analyzed by immunohistochemistry. In these lesions, smooth muscle cells expressed Ebi3 as well as the IL-27alpha/p28 and IL-12alpha/p35 subunits. Primary aortic smooth muscle cells up-regulated Ebi3 in response to proinflammatory stimuli like tumor necrosis factor-alpha and interferon-gamma. Interestingly, pretreatment of these cells with the peroxisome proliferator-activated receptor-gamma agonist rosiglitazone strongly reduced Ebi3 induction. Chromatin immunoprecipitation experiments revealed that this inhibition is due to interference with p65/RelA recruitment to the Ebi3 promoter. Our data support a possible role of Ebi3 in atherogenesis either as homodimer or as IL-27/IL-35 heterodimer, and suggest that Ebi3 could be an interesting target for therapeutic manipulation in atherosclerosis.
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PMID:Epstein-barr virus-induced gene-3 is expressed in human atheroma plaques. 1955 16

Atherosclerosis is a complex, multifactorial disease. Several studies have reported a possible association between infection with microbial agents and atherogenesis. Chlamydia pneumoniae (C. pneumoniae), Herpes Simplex Virus 1 (HSV1), Human Cytomegalovirus (HCMV), and Epstein Barr Virus (EBV) have been widely investigated for their possible role in atherosclerosis development, but the results obtained to date are contradictory. The aim of our study is to search DNA of the aforementioned infectious agents by means of Quantitative Real Time PCR in atherosclerotic plaques from carotid arteries obtained from 17 patients. Genomic sequences of C. pneumoniae, HSV1, HCMV were not found in any atherosclerotic lesion. Therefore, our results do not support the hypothesis of an association between these infectious agents and atherosclerosis. Conversely, three patients were found to be positive for EBV DNA, thus indicating that, at least in a limited number of patients, EBV could play a role in atherogenesis.
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PMID:Search for genomic sequences of microbial agents in atherosclerotic plaques. 2149 9

Previous studies indicated that patients with atherosclerosis are predominantly infected by human cytomegalovirus (HCMV), but rarely infected by type 1 Epstein-Barr virus (EBV-1). In this study, atheromas of 30 patients who underwent aortocoronary bypass surgery with coronary endartherectomy were tested for the presence of these two viruses. HCMV occurred in 93.3% of the samples and EBV-1 was present in 50% of them. Concurrent presence of both pathogens was detected in 43.3% of the samples.
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PMID:Detection of human cytomegalovirus and epstein-barr virus in coronary atherosclerotic tissue. 2403 29

The imbalance of anti- inflammatory/pro-inflammatory cytokines plays an important role in the process of atherosclerosis. IL-35 is an anti-inflammatory cytokine comprising the p35 subunit of IL-12 and the subunit Epstein-Barr virus (EBV) -induced gene 3(EBI3). Accumulating evidence showed that IL-35 up-regulates the expression of anti-inflammatory cytokines, induces the generation of CD4 + regulatory T cells, inhibits CD4 + effector T cells response and other target cells activity, and reduces the progression of inflammatory and autoimmune diseases. In addition, it has been found that Ebi3 and p35 strongly coexpressed in human advanced lesions. Therefore, we hypothesize that IL-35 may become a novel target for the treatment of atherosclerosis. Further studies are required to investigate the precise effect and the signaling pathway of IL-35 in atherosclerosis process.
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PMID:IL-35: a potential target for the treatment of atherosclerosis. 2427 81

What's new in internal medicine will be dedicated to three topics: i) inflammatory myopathies constituting a heterogenous group of diseases whose clinical manifestations, immunological abnormalities, treatment response and outcomes vary widely; ii) alterations of gut microbiota contributing to the occurrence or development of a range of conditions, including autoimmune diseases for which further work is necessary to understand the correlation of dysbiosis with these diseases; iii) the reciprocal relationship between obesity, metabolic syndrome, atherosclerosis and autoimmune diseases. New data concerning systemic sclerosis, cutaneous vasculitis, adult Still's disease, autoantibodies anti DFS70, Epstein Barr virus and autoimmune diseases were also highlighted.
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PMID:[What's new in internal medicine?] 3058 54

Interleukin- (IL-) 35, a novel functional cytokine of regulatory T cells (Treg) comprised of the IL-12p35 subunit and the other subunit Epstein-Barr virus-induced gene 3 (EBI3), regulates the activity of CD4+ T cells and macrophages, thereby playing a critical role in inflammatory and autoimmune diseases. Previous studies demonstrated that both recombinant mice and human IL-35 attenuated atherosclerosis in ApoE-/- mice. Additionally, EBI3 deficiency enhanced the activation of macrophages and increased atherosclerotic lesions in LDLR-/- mice. This study generated double-deficient mice for ApoE and IL-12p35 (ApoE-/- IL-12p35-/- mice) and investigated the effect of IL-12p35 deficiency on atherosclerosis. IL-12p35 deficiency alleviated Th1/Th2 imbalance, aggravated Th17/Treg imbalance, and attenuated atherosclerotic plaque formation in ApoE-/- mice. Additionally, exogenous rIL-35 treatment reversed the imbalance of Th17/Treg and attenuated atherosclerosis in ApoE-/- mice. These findings suggest that IL-12p35 deficiency ameliorates atherosclerosis in ApoE-/- mice, partially, via attenuating the Th1/Th2 imbalance, although IL-12p35 deficiency aggravates the Th17/Treg imbalance.
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PMID:Interleukin-12p35 Deficiency Reverses the Th1/Th2 Imbalance, Aggravates the Th17/Treg Imbalance, and Ameliorates Atherosclerosis in ApoE-/- Mice. 3109 11


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