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)

Chlamydia pneumoniae infection has been associated with coronary heart disease. To evaluate the mechanisms of this association, we studied whether chronic C. pneumoniae infection affects serum lipid values similarly to acute infections. Triglyceride, total and HDL cholesterol concentrations, and C. pneumoniae antibodies were measured from paired serum samples of 415 Finnish males taken 3 years apart. Chronic infection, defined as persistent IgG and IgA antibodies, was found in 20%, and the antibodies were negative (IgG < 32 and IgA < 16 in both samples) in 15% of the cases studied. The serum triglyceride and total cholesterol concentrations were higher in the subjects with a chronic C. pneumoniae infection than in the subjects with no antibodies (1.23 versus 1.03 mmol/L and 6.41 versus 6.31 mmol/L, respectively). The HDL cholesterol concentrations and the ratios of HDL cholesterol to total cholesterol were significantly decreased in the subjects with chronic infection (1.24 versus 1.36 mmol/L, P = .026; and 0.19 versus 0.22, P = .018, respectively). Chronic C. pneumoniae infection seems to be associated with a serum lipid profile considered to increase the risk of atherosclerosis. This finding supports the hypothesis that infections play a role in the pathogenesis of atherosclerosis.
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PMID:Chronic Chlamydia pneumoniae infection is associated with a serum lipid profile known to be a risk factor for atherosclerosis. 940 75

The aim of this study was to assess the presence of Chlamydia pneumoniae antibodies in patients with angiographically verified atherosclerotic coronary artery disease. A total of 114 consecutive patients were investigated between April 1995 and June 1996. Patients were divided into two groups: 72 patients with acute myocardial infarction (AMI; 53 men, 19 women, mean age 62.27 +/- 10.1 years), and 42 patients with chronic ischemic heart disease (CAD; 37 men, 5 women, mean age 62.75 +/- 9.2 years). A control group of 50 normal subjects matched for age (mean 62 +/- 9 years), sex, social status and geographical area was used. Identification of Chlamydia pneumoniae was carried out with the microimmunofluorescence method, on two serum samples taken from patients on admission and after 15 days. The IgM, IgG and IgA anti-Chlamydia pneumoniae titers were assessed, values > or = 1:16, > or = 1:32 and > or = 1:8 being respectively considered positive. Acute (IgM > or = 16 or four fold rise of IgG titer) and chronic (IgG > or = 128 e IgA > or = 32 or only elevated IgA titer) infections were analyzed. IgM antibodies were not found in AMI, CAD and control groups. IgG positivity (IgG > or = 32) was found in 38% of the control group, in 58.3% of the AMI group (p < 0.05) and 42.8% of the CAD group (p < 0.01). IgA positivity > or = 8) was found in 22% of the control group, in 31.9% of the AMI group (NS) and in 33.3% of the CAD group (p < or = 0.05). Acute infection was observed in 5.5% of AMI patients and in 12% of CAD patients (NS), whereas no subject of the control group showed these values. Chronic infection was observed in 9.7% of AMI patients and in 16.6% of CAD patients (NS) whereas nobody of the control group showed these values. In conclusion, our results suggest that Chlamydia pneumoniae infection is present only in the AMI and CAD groups. It is possible to suppose that this infection may be linked to atherosclerosis through an endothelial damage or a systemic endogenous procoagulant and inflammatory activity.
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PMID:[Chlamydia pneumoniae infection and cardiac ischemic syndromes]. 992 69

A review on participation of chlamydiae in the origin of the HIV-infection, carcinoma and atherosclerosis. The antibodies against the newly discovered pgp3 protein of C. trachomatis were found in 83-87% of the seropositive HIV patients. The participation of C. trachomatis in the etiology of cervical and ovarian carcinoma has been discussed in a number of articles. Simultaneous examinations along different lines allow the hypothesis, that C. trachomatis acts as a cofactor in the development of ovarian and cervical carcinoma. Chronic infection by C. pneumoniae appears to be one of the risk factors of pulmonary carcinoma. Many papers dealing with the relation of chlamydiae and atherosclerosis have been published. The relation between the chronic C. pneumoniae-infection and atherosclerosis has been assessed serologically and by direct demonstration of chlamydiae in atheromatous plaques.
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PMID:[Chlamydiae--still new surprises]. 1056 17

On a variety of fronts, chronic infection has been found to be significantly associated with the development of atherosclerosis and the clinical complications of unstable angina, myocardial infarction, and stroke. For the most part, these are still just associations. Specific causative relationships on par with that determined between H. pylori and peptic ulcer disease have not yet been established. Potential mechanisms whereby chronic infections may play a role in atherogenesis are myriad. In the case of C. pneumoniae, the effect may result from direct vessel wall colonization, which may damage the vessel directly or indirectly by initiating immunologic responses. In other cases, the effect may simply be that of enhancing the preexisting chronic inflammatory response of the body to standard risk factors, such as hyperlipidemia. Even though the infectious agent may not directly infect the vessel wall, it may perform its critical role from afar. Chronic infection might also influence preexisting plaque by enhancing T cell activation or other inflammatory responses that may participate in the destabilization of the intimal cap. Chronic infection may play a role in the initiation, progression, or destabilization of atherosclerotic plaques. The infectious agents with the most evidence to support a causative role in atherosclerosis include C. pneumoniae and cytomegalovirus. Evidence is mounting for a variety of other potential agents, including H. pylori, various periodontal agents, and even hepatitis A. Future studies are expected to elucidate further the pathophysiologic relationship between chronic infection and atherosclerosis and to evaluate the potential of a variety of treatment approaches, including antibiotics.
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PMID:Chronic infection and coronary artery disease. 1068 31

Chronic infection and inflammation have recently been implicated as important etiologic agents for atherosclerosis in general and, in particular, ischemic heart disease. Several agents have been suggested as possible candidates for the chronic inflammation including cytomegalovirus, Helicobacter pylori and Chlamydia pneumoniae. We hypothesized that a vascular infection with C. pneumoniae may induce a chronic inflammatory reaction in the host vascular tissue and activated inflammatory cells may express inflammatory mediators such as cyclooxygenase-2 (COX-2) and matrix metalloproteinases (MMPs). At first, we evaluated the relationship between C. pneumoniae infection and atherosclerosis indirectly by serologic study, and then, to confirm our hypothesis, we performed an immunohistochemical study of atherosclerotic plaques. The seropositive rate of anti-Chlamydia pneumoniae IgG was higher in the disease group (Group I, 59.8%, n = 254) than in the negative control group (Group III, 47.4%, n = 97) (p = 0.041), but the anti-Chlamydia pneumoniae IgA was not different in seropositivity between the two groups (Group I, 64.6%; Group III, 57.7%). The simultaneous seropositive rates of both IgG and IgA were 56.7% in Group I and 43.3% in Group III (p = 0.033). In subgroups without the conventional risk factors of atherosclerosis, these findings were more prominent. Furthermore, we performed immunohistochemical staining on the atherosclerotic aortic tissues obtained from patients that were seropositive to C. pneumoniae (n = 5), by using antibodies to C. pneumoniae, COX-2, and MMP-9. The immunoreactivity for COX-2 and MMP-9 increased in the atherosclerotic plaques itself, predominantly in the surrounding area of immunoreactive C. pneumoniae. These findings support our hypothesis and C. pneumoniae may participate in a pathogenetic mechanism for atherogenesis or progression of atherosclerosis. The present study may open a promising perspective concerning future therapeutic trials of chronic inflammation related atherogenesis under pathophysiological conditions.
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PMID:Serologic and histopathologic study of Chlamydia pneumoniae infection in atherosclerosis: a possible pathogenetic mechanism of atherosclerosis induced by Chlamydia pneumoniae. 1095 85

Chlamydia pneumoniae has been detected in atherosclerotic plaques by various means. Chlamydiae are able to cause persistent infections. Serologically elevated antibody titers are found in severe chronic obstructive pulmonary disease. In atherosclerosis and pulmonary emphysema, inflammatory reactions can be seen by means of light microscopy. Specimens from patients with obliterative arteriosclerosis undergoing thrombendarteriectomy and with advanced emphysema undergoing lung volume reduction surgery were examined using scanning (SEM) and transmission (TEM) electron microscopy, and using immunofluorescence with monoclonal antibodies and antiserum against chlamydiae. SEM shows spherical bodies (SBs) with a diameter from 0.3 microm to 0.6 microm on the surface of the alveoli and bronchioles, as well as in atherosclerotic plaques. In atherosclerosis and emphysema, SBs reveal a double membrane, adherence to collagen fibers, tissue destruction, as well as intracellular and interstitial localization in TEM. They show in parts a densely packed central structure. SBs are seen both in alpha-1-antitrypsin deficiency emphysema and smoker's emphysema. Using immunofluorescence microscopy, spots are seen in corresponding distributions to the SBs. Morphological findings are typical for aberrant chlamydiae seen in persistent infections. Chronic infection and bacterial colonization associated with progressive disease seems to be relevant not only in atherosclerosis but also in pulmonary emphysema.
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PMID:The role of chlamydia in the pathogenesis of pulmonary emphysema. Electron microscopy and immunofluorescence reveal corresponding findings as in atherosclerosis. 1099 81

The established risk factors for atherosclerosis such as hypertension, smoking, diabetes mellitus, hyperlipidemia, and hyperhomocysteinemia do not explain clinical and epidemiological features of coronary heart disease (CHD). The role of infectious disease as a CHD risk factor may partly explain these features. Chronic infection with various microorganisms, particularly, Chlamydia pneumoniae, Cytomegalovirus (CMV) and Helicobacter pylori may play a role in etiological factors, linking inflammation and atherogenesis. Results from epidemiological studies, pathology of atherosclerotic plaques, animal studies, molecular biology and clinical antibiotic trials indicated a positive association between C. pneumoniae infection and CHD. Chronic infection might also influence preexisting plaque by enhancing T cell activation, which participate in destabilization of intimal cap. However, the exact nature of pathophysiological link between the organisms and CHD remains to be elucidated. Future antibiotic interventional studies may help to further clarify the role of chronic infection and inflammation in CHD.
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PMID:Chronic infections and atherosclerosis. 1200 6

On a variety of fronts, chronic infection has been found to be significantly associated with the development of atherosclerosis and the clinical complications of unstable angina, myocardial infarction, and stroke. For the most part, these relationships are still just associations. Failure to confirm initial reports of serologic associations also has been common. Specific causative relationships on par with that determined between H pylori and peptic ulcer disease have not yet been established. Potential mechanisms whereby chronic infections may play a role in atherogenesis are myriad. In the case of C pneumoniae, the effect may result from direct vessel wall colonization that may damage the vessel either directly or indirectly by initiating immunologic responses. In other cases the effect may simply be that of enhancing the pre-existing chronic inflammatory response of the body to standard risk factors such as hyperlipidemia. Even though the infectious agent may not directly infect the vessel wall, it may perform its critical role from afar. Chronic infection might also influence pre-existing plaque by enhancing T-cell activation or other inflammatory responses that may participate in the destabilization of the intimal cap. Hence chronic infection may play a role either in the initiation, progression, or the destabilization of atherosclerotic plaques. The infectious agents with the most evidence to support an etiologic role in atherosclerosis include C pneumoniae and cytomegalovirus. Evidence is mounting for a variety of other potential agents including other herpes viruses, influenza, other specific bacteria (such as M pneumoniae), and chronic infections with common bacterial agents (periodontal disease, chronic bronchitis, and chronic urinary tract infection, among others) [191]. Future studies are expected to elucidate further the pathophysiologic relationship between chronic infection and atherosclerosis and to evaluate further the potential of a variety of treatment approaches, including antibiotics.
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PMID:Chronic infection and coronary artery disease. 1462 50

Chlamydia pneumoniae and cytomegalovirus (CMV) have been associated with the development of atherosclerosis. Inflammatory stimuli initiate the biosynthesis of fibrinogen, interleukin (IL)-6 and plasminogen activator inhibitor (PAI)-1 in the liver. Chronic infection may perpetuate the inflammatory status. We hypothesized that infection of human hepatocytes with the intracellular pathogens C pneumoniae and CMV accelerates biosynthesis of fibrinogen, IL-6, and PAI-1 but that this biosynthesis can be reduced with the use of azithromycin. HepG2 human hepatocytes were infected with C pneumoniae and CMV in vitro in the presence of 0, 0.016, 0.125, or 1 microg/mL azithromycin. We measured IL-6, PAI-1, and fibrinogen after 24, 48, 72, and 96 hours. C pneumoniae-infected hepatocytes produce IL-6 (2667 +/- 309 pg/mL vs 137 +/- 120 pg/mL in uninfected cells after 96 hours. Incubation with 0.016 microg/mL azithromycin decreased IL-6 levels to a mean of 1516 +/- 402 pg/mL, and incubation with 0.125 and 1 microg/mL azithromycin decreased IL-6 to 871 +/- 364 and 752 +/- 403 pg/mL, respectively. C pneumoniae-induced IL-6 production was time- and dose-dependent. The interaction of C pneumoniae with azithromycin treatment was significant, indicating an inhibitory effect of azithromycin on C pneumoniae-induced IL-6 production. CMV infection did not lead to IL-6 production by hepatocytes. C pneumoniae and CMV infection did not induce any changes in PAI-1 production. Fibrinogen production was increased by CMV infection after 72 hours (838 +/- 88 ng/mL; P <.01) and after 96 hours by infection with both C pneumoniae and CMV (765 +/- 100 and 846 +/- 123 ng/mL, respectively; P <.05). Azithromycin did not suppress CMV- or C pneumoniae-induced fibrinogen production. Moreover, we could not confirm an antiinflammatory effect of azithromycin in experiments with cross-titrations of azithromycin against either IL-1 or IL-6 (P >.05). Azithromycin reduces C pneumoniae-induced IL-6 production, but not fibrinogen production, by human hepatocytes. This is a result of the antimicrobial properties of azithromycin and not a direct antiinflammatory effect.
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PMID:Azithromycin inhibits interleukin-6 but not fibrinogen production in hepatocytes infected with cytomegalovirus and chlamydia pneumoniae. 1525 3

Several parallels exist between preeclampsia and atherosclerosis. Both are multifactorial diseases that share risk factors such as obesity, insulin resistance, lipid abnormalities, and elevated serum homocysteine. There are also similarities in the biochemical changes seen in both diseases, including elevated serum triglycerides, decreased HDL cholesterol and enhanced formation of small, dense LDL particles as well as vascular atherosclerotic lesions. Chronic infection with Chlamydia pneumoniae has been linked to coronary artery disease. This study evaluated a possible link between the incidence of preeclampsia and infection with C. pneumoniae by examining the rate of seropositivity in 81 women with preeclampsia, and 206 women with normal pregnancies. Although our data confirmed well-known risk factors for preeclampsia such as obesity, diabetes, and hypertension, we found no difference in the rate of seropositivity between preeclampsia and normal pregnancy. On the contrary, the presence of chlamydial antibodies was lower in preeclampsia. Multiparous women with preeclampsia showed a significantly lower rate of seropositivity than multiparous normal women and nulliparous preeclamptics. In addition, women with a history of preeclampsia who developed preeclampsia in the current pregnancy also had a significantly lower rate of seropositivity.
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PMID:Preeclampsia and Chlamydia pneumoniae: is there a link? 1536 46


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