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)

There is growing evidence of an association between Chlamydia pneumoniae infection and atherosclerosis. By using polymerase chain reaction (PCR), we detected the presence of C. pneumoniae DNA in 16 of 92 (17%) arterial specimens with severe atherosclerotic lesions, and in 3 of 109 (3%) such specimens with mild atherosclerotic lesions (p < 0.01) from 49 cases with an autopsy diagnosis of cardiac death and 5 patients who underwent vascular reconstructive surgery. 14 of the 54 cases (28%) were C. pneumoniae-positive in at least 1 vascular sample. 12 of the 14 (86%) PCR positive cases were aged 60 y or older. Normal pulmonary artery specimens from 24 autopsy cases, used as a methodological control, tested negative. The levels of low density lipoprotein cholesterol and triglycerides were significantly lower in the PCR-positive cases than in the PCR-negative cases (p < 0.05). Importantly, 11 of the 14 PCR-positive cases had only 1 risk factor for atherosclerotic cardiovascular disease, whereas all PCR-negative cases had multiple risk factors (p < 0.05). Our data support the idea that C. pneumoniae may be involved in the development of atherosclerosis in humans, especially in cases where classic risk factors are not identified to explain the incidence of atherosclerotic vascular disease.
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PMID:Chlamydia pneumoniae DNA is more frequent in advanced than in mild atherosclerosis lesions. 1506 66

Seroepidemiological and histopathological studies have suggested a link of atherosclerosis with chronic Chlamydia pneumoniae infection. The present study was designed to examine the effect of C. pneumoniae on expression of basic fibroblast growth factor (bFGF) and platelet-derived growth factor (PDGF) in human endothelial cells. Using reverse transcription-polymerase chain reaction, immunoblotting and enzyme-linked immunosorbent assay we found stimulation of bFGF expression depending on the number of infecting bacteria and the time of infection as well. This stimulatory effect was diminished by heat and UV light treatment of the chlamydial inoculum, suggesting that viable bacteria but not bacterial LPS may be essential for eliciting this growth factor. In contrast, the expression of both PDGF-A and PDGF-B was not increased following C. pneumoniae infection. This study demonstrates that C. pneumoniae activates endothelial cells to produce bFGF, a growth factor which is linked to the development of atherosclerotic plaques.
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PMID:Growth factor production in human endothelial cells after Chlamydia pneumoniae infection. 1529 54

Association of inflammation with atherosclerosis has been known for many years. Some organisms: Chlamydia pneumoniae, Helicobacter pylori, Cytomegalovirus, Herpesvirus were considered as possible infectious factors responsible for coronary artery disease development. Several studies reported strong association between chronic Chlamydia pneumoniae infection and atherosclerosis. In this review we presented clinical evidence for and against the hypothetical association between coronary arterial disease and Chlamydia pneumoniae.
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PMID:[Atherosclerosis and inflammation--role of chlamydia pneumoniae infection what do we know to date?]. 1530 23

Chronic Chlamydia pneumoniae infection and autoimmunity to heat shock protein 60 (Hsp60) have both been documented to be associated with atherosclerosis. Herein, we studied the effects of C. pneumoniae infection and a diet with a low-cholesterol supplement on the development of autoantibodies to mouse Hsp60 and early lipid lesions in the aortic valve of C57BL/6JBom mice. In addition, pulmonary infection was investigated. C57BL/6JBom mice were given one to three C. pneumoniae inoculations and fed either a regular diet or a diet enriched with 0.2% cholesterol. Autoantibody responses against mouse Hsp60 developed in both diet groups when the mice were infected with C. pneumoniae and in uninfected mice fed a cholesterol-enriched diet. C. pneumoniae infections increased subendothelial foam cell accumulation in mice on a 0.2% cholesterol-enriched diet (p = 0.022), without apparent hypercholesterolemia. These in vivo data suggest that autoantibodies against mouse Hsp60 develop as a consequence of cholesterol feeding and repeated C. pneumoniae infections. Further, infectious burden increased early lipid lesions in C57BL/6JBom mice fed a cholesterol-enriched diet.
Atherosclerosis 2004 Dec
PMID:Heat shock protein 60 autoimmunity and early lipid lesions in cholesterol-fed C57BL/6JBom mice during Chlamydia pneumoniae infection. 1553 Sep 6

Chlamydia pneumoniae has been linked with increased risk of cardiovascular disease, but data on stroke are sparse. We examined whether seropositivity to Chlamydia pneumoniae was associated with the risk of ischemic stroke in a nested case-control study. Data on Chlamydia pneumoniae serology, lifestyle factors, and medical history were obtained at baseline. Verified cases (n = 254) were compared with gender- and age-matched controls (n = 254). Positive IgA (> or = 1:16) or IgG (> or = 1:64) titers were associated with an increased risk of acute ischemic stroke, i.e. adjusted odds ratios (ORs) were 1.54 (95% confidence interval, CI: 0.96-2.47) and 1.28 (95% CI: 0.83-1.95). The adjusted OR was 1.77 (95% CI: 1.04-3.00) when both titers were elevated. The highest point estimates were seen for ischemic stroke due to large-artery atherosclerosis, adjusted OR: 6.32 (95% CI: 0.76-52.61) (IgG (> or = 1:64)). No clear associations were found for other types of ischemic stroke. The strength of the association varied depending on gender and the chosen cut-off values for the antibody titers. These results partly support the hypothesis that serologic evidence of Chlamydia pneumoniae infection may be associated with an increased risk of ischemic stroke. However, the risk may differ according to gender, subtype of ischemic stroke, and cut-off value of antibody titers.
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PMID:Chlamydia pneumoniae seropositivity and risk of ischemic stroke: a nested case-control study. 1575 5

Chlamydia pneumoniae infection has been often associated with several chronic diseases including asthma and chronic obstructive pulmonary diseases (COPD). The spectrum of Chlamydia pneumoniae infection has been expanded to the association with coronary heart disease (CHD). In Morocco, the implication of Chlamydia pneumoniae infection in these pathologies is unknown. The aim of our study was to determine the relationship between infection with Chlamydia pneumoniae and respiratory pathology and atherosclerosis. The patients were from two departments (department of respiratory disease and of cardiology), and presented exacerbation of COPD and asthma or atherosclerosis. The mean age was 45 years a with a 1.7 sex ratio for the first population and 61 years with a 1.4 sex ratio for the second population. Serological diagnosis of Chlamydia pneumoniae infection has been determined by microimmunofluorescence (MIF). All samples were tested for anti-Chlamydia pneumoniae IgG, IgA and IgM. In the first group, we found 42 % positive for IgG, 11 % for IgA, and no case for IgM. In the second group the presence of anti-Chlamydia pneumoniae IgG was observed in 67.5 % cases, IgA in 16.5 % cases and IgM in 2 % cases, 14 % of patients had negative serology for IgA, IgG, and IgM. Our results are in accord to those reported by other studies. According to these results, it seems that a certain degree of association exists between Chlamydia pneumoniae infection and exacerbation of COPD, asthma and atherosclerosis which should be of importance on a therapeutic point of view.
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PMID:[Part of Chlamydia pneumoniae in atherosclerosis and exacerbation of chronic obstructive pulmonary disease and asthma]. 1577 75

Atherosclerosis is increasingly viewed as an inflammatory process. A number of infectious agents have been implicated in the pathogenesis of coronary artery disease. Chlamydia pneumoniae has been the most popular and well-studied of these pathogens. It is difficult to prove a causal relationship which requires the fulfillment of Koch's postulates, first developed in the late 1800s, to establish an infectious agent as the cause of a disease process. This paper reviews the evidence for and against Chlamydia pneumoniae infection as a contributing factor to atherosclerosis disease. It examines seroepidemiologic and histopathologic studies as well as animal models using Koch's postulates and then provides an analysis of current clinical trial data.
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PMID:Chlamydia pneumoniae and atherosclerosis: from Koch postulates to clinical trials. 1599 Nov 52

Recent evidence has suggested an association between Chlamydia pneumoniae infection and coronary atherosclerosis. A significant association has also been detected between heat shock protein (HSP) 60 antibody and the severity of coronary atherosclerosis. The aim of this study was to define the relationship between instability of ischemic heart disease (IHD) and serum levels of HSP60 and C. pneumoniae antibodies. Blood samples for the measurement of serum antibody titers were obtained from 1131 patients with ischemic heart disease (65+/-9 years; male/female, 828/303) and 127 non-IHD controls with normal coronary arteries (64+/-9 years; male/female, 60/67) on the day of cardiac catheterization. The serum levels of anti-human HSP60 IgG antibody and anti-chlamydial IgM, but not IgG or IgA, antibody were significantly higher in ACS patients than in stable IHD patients or controls. These results suggest that acute C. pneumoniae infection with HSP60-related immunological responses may contribute to the pathophysiology of acute coronary syndromes.
Atherosclerosis 2005 Nov
PMID:Acute Chlamydia pneumoniae infection with heat-shock-protein-60-related response in patients with acute coronary syndrome. 1621 93

Although it has been suggested that cardiovascular disease incidence is increased among atomic bomb survivors, the existence of a causal relationship between radiation exposure and atherosclerosis is unclear. Microbial infections, including those caused by Chlamydia pneumoniae, Helicobacter pylori and cytomegalovirus, have recently been implicated in atherosclerosis. Since immune function is somewhat impaired among atomic bomb survivors, their immune defense against such infections might be diminished. To investigate this possibility, we measured antibody levels to the above microorganisms in the sera of survivors. We found that the levels of IgG and IgA antibodies to Chlamydia pneumoniae decreased significantly with radiation dose, whereas the levels of IgG antibodies to Helicobacter pylori or cytomegalovirus remained unchanged. The inflammation marker C-reactive protein was significantly and positively associated with level of antibodies to Chlamydia pneumoniae only in heavily exposed (>or=1000 mGy) survivors. These results may suggest that among atomic bomb survivors, immune response to Chlamydia pneumoniae is diminished and chronic inflammatory reactions related to Chlamydia pneumoniae infection are present.
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PMID:Levels of antibodies to microorganisms implicated in atherosclerosis and of C-reactive protein among atomic bomb survivors. 1688 37

Chlamydia pneumoniae infection may play a role in the pathogenesis of atherosclerosis. In this study, an oligonucleotide microarray was utilized to examine the transcriptional response of human aortic smooth muscle cells (AoSMC) to C. pneumoniae infection. Alteration of mRNA expression in 71 out of 780 genes was detected at 24 h after infection. Among the down-regulated genes, platelet-derived growth factor receptor-beta (PDGFR-beta) was identified as a target for further analysis because the PDGF system is involved in the fibroproliferative response of SMC in atherogenesis. Reverse transcriptase PCR analysis demonstrated that C. pneumoniae inhibits the up-regulation of PDGFR-beta mRNA occurring in AoSMC after mock infection. PDGFR-beta protein synthesis was examined by immunoblotting and fluorescence-activated cell sorting. Compared with mock-infected cells, the amount of receptor protein was reduced at 24, 48, and 72 h after infection. Diminished PDGFR-beta synthesis in infected cultures was accompanied by the suppression of AoSMC growth following PDGF-BB stimulation. The interference of C. pneumoniae with PDGFR-beta expression may result in decreased SMC proliferation in atherosclerotic plaques, thereby affecting the development and stability of advanced lesions.
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PMID:Chlamydia pneumoniae infection of aortic smooth muscle cells reduces platelet-derived growth factor receptor-beta expression. 1772 56


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