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)

Chronic Chlamydia pneumoniae infection has been associated with atherosclerosis by seroepidemiological studies. Further, acute bacterial infections are known to influence lipid metabolism. To clarify the possible pathogenetic mechanisms of this association, we studied serum lipids and the C. pneumoniae IgG antibody titers of 1,053 males who participated in the reindeer herders health survey in Northern Finland in 1986-1989. The mean age of the study group was 47 years (range 20-87). When comparing nonsmoking C. pneumoniae antibody-positive (IgG > or = 32) subjects to those with no antibodies, the age-adjusted mean concentration of triglycerides was increased (1.34 vs. 1.04 mmol/l; p = 0.03) and high-density lipoprotein (HDL) was decreased (1.24 vs. 1.35 mmol/l; p < 0.001). HDL:total cholesterol ratio was also decreased (0.20 vs. 0.23; p = 0.01). In smokers changes were very similar, but not statistically significant. Thus, C. pneumoniae antibodies seem to correlate with an altered serum lipid profile considered to increase the risk of atherosclerosis. This finding supports the proposal that infections, in this case C. pneumoniae infection, may play a role in the pathogenesis of atherosclerosis.
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PMID:Chlamydia pneumoniae antibodies associated with altered serum lipid profile. 1009 1

Much of the published data suggest a link between herpes infection and atherosclerosis, as well as herpes infection and restenosis. Mechanistically, herpesvirus has been shown to promote inflammation, thrombin generation and platelet binding, and infected cells have been shown to be resistant to apoptosis. There is also good evidence of a link between Chlamydia pneumoniae infection and atherosclerosis. In preliminary studies, antichlamydial antibiotic intervention has been shown to reduce significantly the incidence of cardiac events in patients with coronary artery disease and in myocardial infarction survivors.
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PMID:Infectious agents that play a role in atherosclerosis and vasculopathies. What are they? What do we do about them? 1035 Jun 77

Accumulating evidence supports an association between Chlamydia pneumoniae infection and atherosclerosis. To determine whether there is a causal relationship, the effects of chronic infection with C. pneumoniae on the development of atherosclerosis in apolipoprotein E (apoE)-deficient mice were evaluated. Eight-week-old male apoE-deficient mice were inoculated intranasally with C. pneumoniae three times, at 8, 9, and 10 weeks of age. The combined area of atherosclerotic lesions in the lesser curvature of the aortic arch was measured en face by computer-assisted morphometry. The lesion area was 2.4-fold greater (P=.05) at 16 weeks of age and 1.6-fold greater (P=.05) at 20 weeks of age in infected mice than in control mice. There were no differences in total plasma cholesterol levels between groups. This study demonstrates that C. pneumoniae infection accelerates the progression of atherosclerosis in the aortic arch of apoE-deficient mice.
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PMID:Chlamydia pneumoniae infection accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice. 1035 89

Chlamydia pneumoniae causes respiratory tract infections, and it is transmitted by air and fomites. It is probably more frequent than it is described, due to asymptomatic or mild symptomatic patients. They respond to macrolides, tetracyclines and quinolones, though patients may recover slowly. An increase of the incidence of pneumonia, caused by Chlamydia pneumoniae, is shown in recent multicenter surveys, being even more frequent than Streptococcus pneumoniae and Mycoplasma pneumoniae. Recently it has been demonstrated an association between coronary artery disease and atherosclerosis with Chlamydia pneumoniae infection. Special attention must be paid to the cardiovascular complications of Chlamydia pneumoniae. We describe six clinical cases of Chlamydia pneumoniae pneumonia in which two of them suffered from ischemic artery disease as a complication of the infection.
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PMID:[Chlamydia pneumoniae pneumonia]. 1042 Sep 52

Possible causal relationship between development of atherosclerosis and Chlamydia pneumoniae infection is discussed. If the hypothesis is verified, antibiotics will play important role in the treatment of this artery disease.
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PMID:[Infection hypothesis for the pathogenesis of atherosclerosis--caused by Chlamydia pneumoniae?]. 1049 68

Recent epidemiological studies have demonstrated the association between Chlamydia pneumoniae infection and coronary atherosclerosis. However, the relationship is less clear in the Japanese population. Serum IgA and IgG antibodies to Chlamydia-specific lipopolysaccharide were measured by enzyme-linked immunosorbent assay in 152 consecutive patients(112 males, 40 females, mean age 57 years)who underwent coronary angiography. Patients(n = 123)with coronary artery disease(CAD)were defined as having more than 50% diameter stenosis in at least one major coronary artery. The control group(n = 29) had normal coronary angiograms. In the CAD group, there was a high tendency of prevalence of IgA(20% vs 7%, p = 0.08)and IgG(54% vs 34%, p = 0.052). Prevalence of either IgA or IgG was significantly higher (59% vs 38%, p = 0.045) compared with the control group. Although the index of IgA antibody was not significantly different between the CAD and control groups(median 0.52 vs 0.36, p = 0.19), the index of IgG antibody was significantly higher in the CAD group than in the control group(median 1.29 vs 0.82, p = 0.026). The odds ratios for CAD were 3.4[95% confidence interval(CI)0.6-18.7]for the prevalence of IgA, 2.3(95% CI 0.9-5.2)for the prevalence of IgG, and 2.3(95% CI 1.0-5.2)for the prevalence of either IgA or IgG. Patients with CAD tended to have high prevalence of antibodies to Chlamydia spp, and these findings suggest an association between chlamydial infection and coronary atherosclerosis in the Japanese population.
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PMID:[Association between chlamydial infection and coronary artery disease]. 1057 34

There is widespread consensus that atherosclerosis is an inflammatory disease. Between possible pathogenetic mechanisms, infective hypothesis has received increasing attention. Researches have recently focused their attention on the role of Chlamydia pneumoniae, a gram-negative intracellular organism, as infection by this bacterium has been demonstrated frequently associated with atherosclerosis. This review attempts to analyze and critically evaluate available data of the literature about the association between Chlamydia pneumoniae and atherosclerosis in order to provide updated elements of judgement concerning a possible future revolutionary scenario: the consideration of atherosclerosis as an infective disease, susceptible to prevention and treatment by means of antimicrobial therapy. More than twenty sero-epidemiological studies have found a two-fold or greater risk of cardiovascular events in subjects with serological evidence of Chlamydia pneumoniae infection. The organism has been identified in over 50% of atherosclerotic plaques examined by various histopathological techniques, while it has been only rarely found in normal artery tissues; moreover, viable Chlamydia pneumoniae has recently been isolated from coronary and carotid atherosclerotic plaques. Several experimental studies have shown that the biological properties of Chlamydia pneumoniae can explain its potential role in initiating and/or modulating plaque formation. The most relevant issue, i.e. the possibility of preventing or slowing progression of the disease with antimicrobial treatment, is still unsolved: only data from experimental studies on animals and four small intervention trials on humans are available, and their encouraging results require confirmation in larger prospective studies. In conclusion, while the association between Chlamydia pneumoniae and atherosclerosis seems to be established, it is still uncertain whether or not the organism plays a causal role in atherosclerosis and its complications. It is hoped that the results of wide scale clinical intervention trials with antibiotics for the secondary prevention of atherosclerotic diseases now in progress will clarify this problem.
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PMID:[Chlamydia pneumoniae and atherosclerosis]. 1063 18

Linkage between Chlamydia pneumoniae infection and atherosclerosis has been confirmed in several studies, but the precise role of this organism in the disease process is not known. We investigated the relation and reactivity of T lymphocytes of human carotid plaques to C pneumoniae antigens. Tissue specimens were obtained from 17 patients who underwent carotid endarterectomy. Immunohistological staining and/or in situ hybridization revealed the presence of C pneumoniae in 11 (64%) of the 17 of the cases. Inflammatory infiltration seen in the vessel walls consisted primarily of CD45RO+ T-memory lymphocytes (median 80%, range 50% to 90%), whereas CD20+ B cells and monocytes were in minor proportion. In vivo activated T lymphocytes were propagated from the specimens with interleukin-2, and the antigen specificity of the established T-cell lines (TLLs) was analyzed against C pneumoniae elementary body antigen. TLLs were established from all 17 carotid tissues but none from the control specimens of ascending aorta. C pneumoniae was recognized as a specific T-cell-stimulating antigen in 7 (41%) of 17 cases. Further analyses of the C pneumoniae-reactive TLLs showed that chlamydial 60-kDa heat-shock protein induced specific proliferation in 5 (71%) of 7 cases and revealed 2 haplotype (DRB1*1502 and DQB1*06) binding motifs in human 60-kDa heat-shock protein. C pneumoniae was identified as a specific microbial antigen recognized by 41% of TLLs propagated from in vivo activated plaque T cells. Our results suggests that cell-mediated immunity to C pneumoniae plays a role in the atherosclerotic process and that this response may involve autoimmunity.
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PMID:Detection of Chlamydia pneumoniae-reactive T lymphocytes in human atherosclerotic plaques of carotid artery. 1076 74

Chlamydia pneumoniae infection has been associated with asthma and atherosclerosis. Smooth muscle cells represent host cells for chlamydiae during chronic infection. In this study we demonstrated that C. pneumoniae infection of human smooth muscle cells in vitro increased production of interleukin 6 (IL-6) and basic fibroblast growth factor (bFGF) as shown by reverse transcription-PCR, immunoblotting, and enzyme-linked immunosorbent assay. In contrast, levels of platelet-derived growth factor A-chain mRNA were not affected after infection. The stimulation of bFGF and IL-6 production was most effective when viable chlamydiae were used as inoculum. Furthermore, inhibition of bacterial protein synthesis with chloramphenicol prevented up-regulation of IL-6 and bFGF in infected cells. Addition of IL-6 antibody to infected cultures diminished bFGF expression, indicating involvement of produced IL-6. These findings suggest that chlamydial infection of smooth muscle cells elicits a cytokine response that may contribute to structural remodeling of the airway wall in chronic asthma and to fibrous plaque formation in atherosclerosis.
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PMID:Production of basic fibroblast growth factor and interleukin 6 by human smooth muscle cells following infection with Chlamydia pneumoniae. 1081 22

The obligate intracellular bacterium Chlamydia pneumoniae has been implicated in the pathogenesis of atherosclerosis since viable pathogen has been recovered from plaques. Chlamydiae are epithelial pathogens notorious for causing persistent infection. Atherosclerosis, however, is a chronic inflammatory disease involving mesenchymal cells of the vascular wall. A bacterial contribution to atherosclerosis appears more relevant if the resident mesenchymal cells of the vascular wall that constitute the plaque can support chlamydial infection continuously. Therefore we inoculated immortalized and primary mesenchymal cells with a vascular and a respiratory Chlamydia pneumoniae isolate. Primary human coronary artery endothelial and smooth muscle cells, primary human embryonic fibroblasts as well as the immortalized cell lines were permissive for continuous growth of both strains. Thus, the resident vascular cells that produce the atheromatous plaque can acquire permanent productive. Chlamydia pneumoniae infection. Immortalized monocytic cells and peripheral blood monocytes also supported chlamydial growth, though productive infection ceased after 5 passages. Monocytes/macrophages are not resident cells of the vascular wall but have an active role in plaque formation. Systemic circulation and transendothelial migration makes them a potential vector system for chlamydial distribution. These findings add further plausibility to the hypothesis of a chronic infectious component in the multifactorial condition of atherosclerosis. Further studies must precisely define chlamydial target cells in vivo and differentiate infection in resident cells of the vascular wall from a presence limited to migrating macrophages. Endovascular infection might provide an explanation for unclear phenomena of atherogenesis like mesenchymal cell proliferation and its distinct inflammatory component.
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PMID:Atherogenetically relevant cells support continuous growth of Chlamydia pneumoniae. 1082 41


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