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)

Accumulating evidence suggests that higher antibody titers to heat shock proteins (HSPs) are associated with the development and severity of atherosclerosis. The aim of this study was to evaluate the impact of cardiac rehabilitation therapy (CRT) or stain treatment (STT) or a combination of both (COM) on anti-HSP antibodies in patients with coronary artery disease (CAD) after percutaneous coronary intervention (PCI). Clinical evaluation of subjects was performed both at the commencement and completion of the 14 weeks of treatment. CRT consisted of a supervised 6 weeks of exercise following hospital discharge and 8 weeks of home stay exercise. Patients assigned to statin therapy were treated with 80 mg per day of fluvastatin. Blood samples from 39 patients were analyzed for antibodies to HSP60 and HSP70 by ELISA. Biochemical parameters, including lipids, high-sensitivity C reactive protein (hsCRP), and interleukin-6 (IL-6), were also analyzed. We found that CRT and COM reduced antibody titers to HSP60 and HSP70 in CAD patients (by 3.79 and 10.00% of anti-HSP60, and by 5.74 and 3.45% of anti-HSP70, respectively) but statin treatment reduced only antibody titers to HSP70 (by 3.83%). There was a significant correlation between antibody titers to HSP60 versus HSP70. Considering the fact that antibody titers to HSPs are associated with the autoimmune process in CAD, CRT and COM have greater effects on reduction in autoimmune reaction after PCI than statin treatment. This reduction was accompanied by greater improvements in blood biochemical variables, such as lipids, hsCRP, and IL-6 after CRT and COM.
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PMID:Effect of cardiac rehabilitation and statin treatment on anti-HSP antibody titers in patients with coronary artery disease after percutaneous coronary intervention. 1710 38

Significant associations between atherosclerosis and both Porphyromonas gingivalis, a major periodontopathogen, and the respiratory pathogen, Chlamydia pneumoniae, have been shown. Many individuals with evidence of atherosclerosis demonstrate seropositivity to these pathogens. The aim of the present study was to examine the atherogenic effect of repeated immunizations with either or both of these agents, and to determine if molecular mimicry of bacterial heat-shock protein (HSP), termed GroEL, and host (h) HSP60 was involved. Atherogenesis was examined in apolipoprotein-E-deficient (-/-) mice following intraperitoneal immunizations with P. gingivalis, C. pneumoniae, P. gingivalis, and C. pneumoniae or vehicle. Lesion area in the proximal aorta and levels of serum antibodies to P. gingivalis, C. pneumoniae, and GroEL were measured. The increased pathogen burden of P. gingivalis, but not of C. pneumoniae, enhanced atherosclerosis. hHSP60 was detected in lesions, and in P. gingivalis-immunized mice, lesion development was correlated with anti-GroEL antibody levels, supporting the involvement of molecular mimicry between GroEL and hHSP60.
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PMID:Anti-P. gingivalis response correlates with atherosclerosis. 1718 60

It is becoming increasingly clear that infections and chronic inflammatory conditions, such as periodontitis can be linked with atherosclerotic process. Periodontitis and atherosclerosis have many pathogenetic mechanisms in common. The objective of this based on current knowledge review is to present the putative mechanisms whereby periodontitis which is chronic and inflammatory in nature and initiated by microbial plaque can influence the atherosclerosis. Two main processes in particular are worthy of consideration and may provide the link between these two diseases. Induction of the chronic systemic inflammation has been proposed to be of pathogenetic relevance in the association of infection and atherosclerosis, and may rely in part on the endothelial toxicity of bacterial endotoxin and the action of proinflammatory cytokines (PGE-2, IL-1beta, TNF-alpha). Another well-founded proatherogenetic property of infectious illness may be the induction of autoimmunity and autoagression. It has been suggested that humoral immune cross-reaction of the same antibodies to heat shock proteins (HSP), both bacterial mHSP65 and human endothelial HSP60 may play an important role in the process of vascular endothelial injury. Both of these mechanisms are believed to be a key event in the pathogenesis of artheriosclerosis.
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PMID:[The impact of periodontal infection on systemic inflammatory process and atherosclerosis]. 1744 82

Immunoinflammatory processes due to chronic infection are thought to be one of the definitive atherogenetic processes. Especially, anti-heat shock protein antibodies have been related to the prevalence of disease such as coronary artery disease or cerebral infarction, etc., resulted from atherosclerosis. Furthermore, the presence of HSP60-specific T lymphocytes in circulation may increase the risk of atherosclerosis. We have recently demonstrated the evidences that Helicobacter pylori infection induced atherosclerosis in apoe+/- ldlr+/- mice and that Hp-anti-heat-shock protein specific Th1-dominant immune responses had a major involvement in the progression of atherosclerosis. These cellular immune responses caused autoimmunity against endogenous HSP60 (expressed on the stressed cells of vascular endothelium), due to the molecular mimicry. Therefore, an appropriate treatment with antibiotics or with anti-HSP60 antibodies, which regulates the Th1 induction, could sufficiently reduce the progression of atherosclerosis.
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PMID:Chronic infections and atherosclerosis. 1789 24

It has been demonstrated that atherosclerosis (ATS) is enhanced in autoimmune rheumatic diseases, such as systemic lupus erythematosus (SLE). The reason for this accelerated process is still debatable and, although traditional risk factors are more prevalent in SLE patients than in general population, they do not seem to fully explain the enhanced risk. ATS has the characteristics of an autoimmune chronic disease, involving both the innate and the adaptive immunity. Moreover, it satisfies the four criteria defining an autoimmune disease, proposed by Witebsky and Rose. It has been shown that some autoantibodies, including anti-oxLDL, anti-beta(2)GPI, anti-HSP60/65, and more recently anti-oxLDL/beta(2)GPI, play a key role in the pathogenesis of ATS. However the role of these autoantibodies in accelerated ATS in SLE patients is still controversial. In fact, some of them seem to be proatherogenic and other protective; moreover, it has been demonstrated that induced oral tolerance has a protective role against ATS. We have recently observed that the levels of oxLDL/beta(2)GPI antigenic complexes and their antibodies were higher in patients with SLE than in healthy subjects, but we did not find a clear association between oxLDL/beta(2)GPI complexes and IgG or IgM anti-oxLDL/beta(2)GPI autoantibodies and subclinical ATS in SLE patients. Many other studies are required to explain the role of autoantibodies in the pathogenesis of ATS in SLE patients, because the characteristics of SLE seem to mask their effects for atherogenesis.
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PMID:OxLDL/beta2GPI-anti-oxLDL/beta2GPI complex and atherosclerosis in SLE patients. 1796 26

The combination of HSP60-specific humoral and cellular reactions is handled as the new diagnostic sign, reflecting the risk of the development of atherosclerosis, which is independent of other classic risk factors. Chaperones are identified as important pathogen-related antigens used to design vaccines against atherosclerosis. The high evolutionary homology of HSPs raises the issue on the safety of such vaccines.
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PMID:[Chaperones and their role in atherogenesis]. 1831 55

Many reports regarding the cytotoxicity of antibodies to heat shock protein (HSP) 65/60 have implied the potential disadvantage and risk of HSP65/60-specific Th2 shifting strategy in arresting atherosclerosis. In this study, experiments were specifically designed to investigate the effect of a HSP65-specifc Th1 to Th2 immune shift accompanied with high-titer antibodies on atherosclerosis and explore the proatherogenic cytotoxicity of Th2-deviated anti-HSP65 antibodies to endothelial cells. Rabbits were nasally immunized with a fusion protein HSP65-6 x P277 10 times every other day. Immunologic results, including the repressed T-cell proliferation, increased interleukin-10 production and IgG1-predominated isotype of antibodies, revealed a significant Th1 to Th2 shift of response to HSP65. However, rabbits showed no reduction in atherosclerotic lesions. As a control, HSP65 immunization, which induced no antibodies, obviously attenuated atherosclerosis. Further studies on endothelial cells showed that the Th2-deviated anti-HSP65 antibodies could cross-react with HSP60 highly expressed in stressed cells and mediate damage to cells in the presence of complement. In conclusion, the Th2-deviated antibodies to HSP65 that were induced by over-regulated Th2 shift are cytotoxic to endothelial cells. This proatherogenic effect, in contradiction to the positive impact of Th1 suppression, can eventually invalidate the efficacy of Th2 shift in arresting atherosclerosis.
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PMID:A Th2 immune shift to heat shock protein 65 fails to arrest atherosclerosis: Proatherogenic role of Th2-deviated autoantibodies. 1941 13

Helicobacter pylori (H. pylori) is a predominant pathogen that causes not only gastroduodenal diseases but also extra-alimentary tract diseases. In this study, we demonstrated that H. pylori infection promoted atherogenesis in heterozygous apoe(+/ --) ldlr(+/--) mice. The male mice were fed with high fat diet from the age of 6 weeks. At the age of 16 weeks, development of atherosclerotic lesions was observed in the H. pylori-infected mice, and it seemed to be associated with an elevation of Th1-immune response against H. pylori origin-heat shock protein 60 (Hp-HSP60) and an increment of transendothelial migration of T cells. Subcutaneous immunisation with Hp-HSP60 or H. pylori eradication with antibiotics significantly reduced the progression of atherosclerosis, accompanied by a decline of Th1 differentiation and reduction of their chemotaxis beyond the endothelium. Thus, oral infection with H. pylori accelerates atherosclerosis in mice and the active immunisation with Hp-HSP60 or the eradication of H. pylori with antibiotics can moderate/prevent cellular immunity, resulting in a reduction of atherosclerosis.
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PMID:Regulation of cellular immunity prevents Helicobacter pylori-induced atherosclerosis. 1988 May 62

Chlamydophila pneumonia (C. pneumonia) infection has been associated with the progression of atherosclerosis. It remains unclear, however, whether C. pneumoniae in the absence of an immune response can alone initiate atherogenic events within a complex vessel environment. Left anterior descending coronary arteries isolated from porcine hearts were dissected and placed in culture medium for 72 hours before infection with C. pneumoniae. C. pneumoniae replicated within the arterial wall for the duration of the experiment (up to 10 days). A significant increase in chlamydial-HSP60 protein expression from day 2 to 10 post-infection (pi) indicated the presence of metabolically active C. pneumonia within infected vessels. Significant arterial thickening in infected coronary segments was observed by a considerable decrease in the ratio of lumen to total vessel area (48 +/- 3% at day 4 pi versus 23 +/- 3% at day 10 pi) and a significant increase in the ratio of media to luminal area (113 +/- 16% at day 4 pi versus 365 +/- 65% at day 10 pi). Structural changes were accompanied by an up-regulation of host HSP60 and proliferating cell nuclear antigen expression levels. Immunohistochemical staining confirmed proliferating cell nuclear antigen expression to be primarily localized within smooth muscle cells of the medial area. These results demonstrate that C. pneumoniae infection can stimulate arterial thickening in a complex vessel environment without the presence of a host immune response and further supports the involvement of HSP60 in this action.
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PMID:Chlamydophila pneumoniae infection leads to smooth muscle cell proliferation and thickening in the coronary artery without contributions from a host immune response. 2001 96

Cariogenic and periodontal pathogens are thought to be etiological factors in the development of cardiovascular disease. We assessed the involvement of the periodontal pathogen Aggregatibacter actinomycetemcomitans and cariogenic pathogen Streptococcus mutans in the development of atherosclerosis in apolipoprotein E-deficient spontaneously hyperlipidemic (Apoe(shl)) mice. The mice were treated intravenously with A. actinomycetemcomitans HK1651, S. mutans GS-5, or phosphate-buffered saline three times a week for 3 weeks and killed at 15 weeks of age. The areas of the aortic sinus that were covered with atherosclerotic plaque were significantly larger in Apoe(shl) mice challenged with A. actinomycetemcomitans compared with S. mutans- or vehicle-challenged mice. Aggregatibacter actinomycetemcomitans challenge increased serum high-sensitive C-reactive protein and lipopolysaccharide levels. Bacterial DNA was detected in the blood, heart, and spleen, but not in the liver. Furthermore, serum interleukin-6 (IL-6), IL-8, tumor necrosis factor alpha, and MCP-1 levels and Toll-like receptor (TLR)2, TLR4, ICAM-1, E-selectin, P-selectin, LOX-1, HSP60, CCL19, CCL21, CCR7, and MCP-1 expressions in the aorta were significantly increased in mice challenged with A. actinomycetemcomitans. These results suggest that systemic infection with A. actinomycetemcomitans accelerates atherosclerosis in Apoe(shl) mice by exposing the whole microorganisms or their products, followed by initiating inflammation. Increases in proatherogenic factors may explain the aggravation of atherosclerosis by A. actinomycetemcomitans infection.
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PMID:Aggregatibacter actinomycetemcomitans accelerates atherosclerosis with an increase in atherogenic factors in spontaneously hyperlipidemic mice. 2048 27


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