Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of circulating immune complexes (IC) was studied using two detection methods specific for chlamydial lipopolysaccharide (LPS) in paired serum samples of 44 patients (30 men and 14 women) with acute myocardial infarction (AMI). Forty-four random controls were individually matched for locality, age and sex with the AMI patients. As specificity controls for the IC assays single serum samples from 29 patients with diseases characterized by the presence of circulating IC were used. Fifty-seven per cent of AMI patients, 12% of their random controls and 10% of the patient controls were shown to have chlamydial LPS-specific immune complexes in their sera (P less than 0.0001, AMI versus random and patient controls). This finding provides further evidence of the possible association of chronic chlamydial infection with AMI.
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PMID:Circulating immune complexes containing chlamydial lipopolysaccharide in acute myocardial infarction. 207 46

Paired sera from 40 male patients with acute myocardial infarction (AMI), 30 male patients with chronic coronary heart disease (CCHD), and 41 controls, matched for sex, age, time, and locality were investigated for antibodies to a novel type of Chlamydia sp, TWAR, and to chlamydial lipopolysaccharide (LPS) group antigen. 27 patients with AMI (68%), and 15 (50%) patients with CCHD had raised IgG (greater than or equal to 128) and/or IgA (greater than or equal to 32) titres in the microimmunofluorescence test with chlamydia TWAR. Both frequencies were significantly higher than in the controls (7, 17%). 26 (68%) of 38 patients with AMI also showed a significant seroconversion in enzyme immunoassay with LPS antigen; this response was absent in all patients with CCHD and all but 1 of the controls. Chronic chlamydial infection could be a factor in the pathogenesis of cardiovascular diseases.
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PMID:Serological evidence of an association of a novel Chlamydia, TWAR, with chronic coronary heart disease and acute myocardial infarction. 290 92

To elucidate the role of monocytes in the cytokine system in acute myocardial infarction (AMI), we examined the time courses of plasma concentrations and generation capacities of monocyte-related cytokines in 17 consecutive patients with uncomplicated AMI (from day 1 to 28) and in 10 control subjects. The concentrations of monocyte-related cytokines were measured by enzyme immunoassay with horseradish peroxidase. Cytokine generation capacity was evaluated by cytokine concentrations in the culture solution 24 hours after incubation of 0.5 ml whole blood with 5 micrograms lipopolysaccharide. Two distinct patterns of increases in the cytokine concentrations were noted: transient (plasma interleukin [IL]-6) and sustained (plasma macrophage colony-stimulating factor and generation capacities of IL-1 alpha, IL-6, granulocyte colony-stimulating factor, and tumor necrosis factor alpha). There was no significant increase in the concentrations of other cytokines. These results indicate that the concentrations of the monocyte-related cytokines dynamically change during the course of AMI, suggesting that they may contribute to the inflammatory and subsequent proliferative responses in AMI.
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PMID:Monocyte-related cytokines in acute myocardial infarction. 766 Oct 59

While early observations on the possible connection between chlamydia and arteriosclerosis remain unnoticed, it was found recently that in acute myocardial infarction (AMI) a sero response to an epitope of chlamydial lipopolysaccharide (LPS) could be demonstrated in about 70% of cases. Moreover, steadily elevated titres against Chlamydia pneumoniae in patient sera pointed to a possibility that chronic infection due to the agent was exacerbated in AMI. This assumption has been further supported by the finding of (a) elevated C. pneumoniae antibody titres in coronary heart disease patients in several studies, (b) the presence of immune complexes containing chlamydial LPS in acute AMI cases and their formation of antigen excess followed a month later by antibody excess, (c) the presence of antibodies to C. pneumoniae proteins in immune complexes in chronic coronary heart disease. The presence of elevated antibody titres and/or immune complexes containing chlamydial LPS was a significant independent risk factor (up to 2.6, CL, 1.3 to 5.2) for AMI 3-6 months before cardiac incidents in the Helsinki Heart Study. The odds ratio was especially significant (up to 7.2, CL, 1.4 to 35) if the cohort on cholesterol-lowering drug was followed.
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PMID:Chlamydia pneumoniae infection as a risk factor in acute myocardial infarction. 813 91

Chlamydia pneumoniae is frequently found in atherosclerotic lesions, and high titers of specific antibodies are associated with increased risk for acute myocardial infarction. However, a causative relation has not been established yet. We performed a prospective study of 93 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) to investigate whether angioplasty influences Chlamydia-specific antibody titers and whether there is an association with restenosis. Blood samples were obtained before and 1 and 6 months after angioplasty. Antibodies against chlamydial lipopolysaccharide and against purified C. pneumoniae elementary bodies were measured by enzyme-linked immunosorbent assay (ELISA). After angioplasty, the prevalence of antibodies to lipopolysaccharide rose from 20 to 26% for immunoglobulin A (IgA), from 53 to 64% for IgG, and from 2 to 7% for IgM (P = 0.021, 0.004, and 0.046, respectively). There was a rapid increase of mean antibody titers of all antibody classes within 1 month of PTCA. During the following 5 months, antibody titers decreased slightly but were still higher than baseline values. Results of the C. pneumoniae-specific ELISA were essentially the same. The rise of anti-Chlamydia antibodies was not caused by unspecific reactivation of the immune system, as levels of antibodies against cytomegalovirus did not change. Neither seropositivity nor antibody titers were related to restenosis. However, increases in mean IgA and IgM titers were restricted to patients who had suffered from myocardial infarction earlier in their lives. In conclusion, we show that PTCA induces a stimulation of the humoral immune response against C. pneumoniae. These data support the idea that plaque disruption during angioplasty might make hidden chlamydial antigens accessible to the immune system.
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PMID:Coronary angioplasty induces rise in Chlamydia pneumoniae-specific antibodies. 1007 19

The effect of lipopolysaccharide (LPS, endotoxin) on low density lipoprotein (LDL) oxidative modification by copper ions, endothelial and smooth muscle cells was studied by determination of the level of lipid peroxidation products (thiobarbituric acid reactive substances or TBARS), the diene level and the electrophoretic mobility of the LDL particle. LPS 25-75 microg/ml induced a dose-dependent increase in LDL oxidation by copper ions, endothelial and smooth muscle cells. At 75 microg LPS/ml, the TBARS content was 1.9, 1.6, and 1.8-fold increased, respectively. The LDL degradation by J774 macrophage-like cells was concomitantly stimulated. Preincubation of the LDL particle with LPS induced a marked increase in the subsequent LDL oxidative modification either by copper ions or by endothelial and smooth muscle cells. In addition, pretreatment of endothelial and smooth muscle cells with LPS also induced an enhancement of LDL oxidative modification performed in the absence of LPS. This effect was accompanied by a parallel increase in superoxide anion release by the cells. These results point at one of the mechanisms involved in the described association between bacterial infection and acute myocardial infarction as well as coronary heart disease.
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PMID:Lipopolysaccharide enhances oxidative modification of low density lipoprotein by copper ions, endothelial and smooth muscle cells. 1020 81

Endotoxin is a biologically active substance that has a lipopolysaccharide structure. It is found in the cell walls of microorganisms, principally gram-negative bacteria. By contacting with the cell, endotoxin enhances immunity. The findings suggest that acute myocardial infarction (AMI) occurs due to low immunity that remains the same at week 3 of the disease, thus the levels of antiendotoxin agents may be used in predicting AMI.
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PMID:[On possible prognostic values of anti-endotoxin immunological parameters in acute myocardial infarction]. 1083 83

About 70% of persons with acute myocardial infarction (AMI) show a seroresponse to a chlamydial lipopolysaccharide (LPS) epitope. Elevated titers against Chlamydia pneumoniae in sera from such patients point to an exacerbation in a chronic infection as does a change in the nature of immune complexes containing chlamydial LPS. The presence of antibodies to C. pneumoniae proteins in immune complexes suggests an intimate association of the pathogen with the vascular system. In the first prospective study, elevated antibody titers or immune complexes containing chlamydial LPS were an independent significant risk factor (odds ratio, </=2.6) for AMI 3-6 months before the cardiac incident. The majority of later seroepidemiologic studies have verified the association. However, since serologic markers for C. pneumoniae infection also seem to be associated with uncomplicated atherosclerosis and other chronic conditions, their predictive value for cardiac events is small.
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PMID:Epidemiologic association of Chlamydia pneumoniae and atherosclerosis: the initial serologic observation and more. 1083 25

Chlamydia infection of the cardiovascular system is associated with pericarditis, endocarditis and myocarditis. Chlamydia particles can also be observed in damaged heart valves. There is now good evidence that the lesions of arteriosclerosis and aortic aneurysm as well as valvular disease may be associated with C. pneumoniae infection. Patients with acute myocardial infarction show seroconversion against Chlamydia lipopolysaccharide. In a prospective study of 4000 healthy hypercholesterolemic men, signs suggestive of chronic C. pneumoniae infection increased the risk of a cardiac event three---fold. This risk factor is synergistic with the smoking risk. Immunohistochemistry also demonstrated Chlamydia lipopolysaccharide in samples of aortic aneurysm. Chlamydial inflammation may play a role in the oxidation of low density lipoprotein in atherosclerotic lesions.
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PMID:Chlamydia pneumoniae and cardiovascular diseases. 1186 90

Inflammation is a major contributing factor to atherosclerotic plaque development and ischemic heart disease. PTX3 is a long pentraxin that was recently found to be increased in patients with acute myocardial infarction. Because tissue factor (TF), the in vivo trigger of blood coagulation, plays a dominant role in thrombus formation after plaque rupture, we tested the possibility that PTX3 could modulate TF expression. Human umbilical vein endothelial cells, incubated with endotoxin (lipopolysaccharide) or the inflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha, expressed TF. The presence of PTX3 increased TF activity and antigen severalfold in a dose-dependent fashion. PTX3 exerted its effect at the transcription level, inasmuch as the increased levels of TF mRNA, mediated by the stimuli, were enhanced in its presence. The increase in mRNA determined by PTX3 originated from an enhanced nuclear binding activity of the transacting factor c-Rel/p65, which was mediated by the agonists and measured by electrophoretic mobility shift assay. The mechanism underlying the increased c-Rel/p65 activity resided in an enhanced degradation of the c-Rel/p65 inhibitory protein IkappaBalpha. In the area of vascular injury, during the inflammatory response, cell-mediated fibrin deposition takes place. Our results suggest that PTX3, by increasing TF expression, potentially plays a role in thrombogenesis and ischemic vascular disease.
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PMID:Long pentraxin PTX3 upregulates tissue factor expression in human endothelial cells: a novel link between vascular inflammation and clotting activation. 1200 90


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