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 incidence of Chlamydia pneumoniae infection was determined in patients with chronic obstructive pulmonary diseases (COPD) by prospective serial serology. Chlamydia-specific IgG, IgM and IgA antibodies were detected with a recombinant DNA lipopolysaccharide (LPS) ELISA as well as with a micro-immunofluorescence (MIF) assay with C. pneumoniae elementary bodies. From 271 consecutive COPD patients who visited the outpatient clinic of the department of pulmonary diseases (211 males, 60 females, age range 34-88 years, mean age 66 SD 10 years), blood samples (n = 1058) were taken every 2-7 months; the observation period ranged from 3 to 19 months (mean 15 SD 4). The prevalence of chlamydial IgG was 72% with the MIF and 53% with the rDNA LPS ELISA. More than 90% of the COPD patients had no significant changes in their chlamydia-specific IgG, IgA and IgM titres in either test during the observation period. Seven (3%) patients had MIF results indicating acute C. pneumoniae infection during their surveillance period, of whom five were confirmed by rDNA LPS ELISA. Eleven (4%) additional patients were infected during observation, as determined by rDNA LPS ELISA only. These patients had significantly elevated C. pneumoniae-specific IgG and IgA MIF titres, as compared with the patients without infection. All 18 patients with serological evidence of acute infection during their surveillance period were re-tested in a commercial MIF test that can distinguish between C. pneumoniae, C. trachomatis and C. psittaci LPS-specific antibodies, but no evidence of C. trachomatis or C. psittaci infection was found. The incidence of chlamydial infection was 2.2 and 5.3/100 person-years, when diagnosed by MIF and rDNA LPS ELISA, respectively. It is concluded that the rDNA LPS chlamydia assay may currently be the most sensitive serological tool for diagnosing recent respiratory chlamydia infections and that C. pneumoniae infection occurs frequently in COPD patients.
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PMID:Diagnosis of Chlamydia pneumoniae infection in patients with chronic obstructive pulmonary disease by micro-immunofluorescence and ELISA. 936 38

Chlamydia pneumoniae infection is associated with atherosclerotic heart and vessel disease, but a causal relationship between this pathogen and the disease process has not been established. Recently, it was reported that C. pneumoniae induces human macrophage foam cell formation, a key event in early atheroma development, suggesting a role for the organism in atherogenesis. This study further examines C. pneumoniae-induced foam cell formation in the murine macrophage cell line RAW-264.7. Infected RAW cells accumulated cholesteryl esters when cultured in the presence of low-density lipoprotein in a manner similar to that described for human macrophages. Exposure of C. pneumoniae elementary bodies to periodate, but not elevated temperatures, inhibited cholesteryl ester accumulation, suggesting a role for chlamydial lipopolysaccharide (cLPS) in macrophage foam cell formation. Purified cLPS was found to be sufficient to induce cholesteryl ester accumulation and foam cell formation. Furthermore, the LPS antagonist lipid X inhibited C. pneumoniae and cLPS-induced lipid uptake. These data indicate that cLPS is a C. pneumoniae component that induces macrophage foam cell formation and suggest that infected macrophages chronically exposed to cLPS may accumulate excess cholesterol to contribute to atheroma development.
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PMID:A Chlamydia pneumoniae component that induces macrophage foam cell formation is chlamydial lipopolysaccharide. 978 5

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

Data from a spectrum of epidemiologic, pathologic, and animal model studies show that Chlamydia pneumoniae infection is associated with coronary artery disease, but it is not clear how the organism may initiate or promote atherosclerosis. It is postulated that C. pneumoniae triggers key atherogenic events through specific virulence determinants. C. pneumoniae induces mononuclear phagocyte foam cell formation by chlamydial lipopolysaccharide (cLPS) and low-density lipoprotein oxidation by chlamydial hsp60 (chsp60). Thus, different chlamydial components may promote distinct events implicated in the development of atherosclerosis. Data implicating cLPS and chsp60 in the pathogenesis of atherosclerosis are discussed and novel approaches are presented for attempting to elucidate how these putative virulence determinants signal mononuclear phagocytes to modulate lipoprotein influx and modification.
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PMID:Chlamydial virulence determinants in atherogenesis: the role of chlamydial lipopolysaccharide and heat shock protein 60 in macrophage-lipoprotein interactions. 1083 44

Recent studies suggest an association between Chlamydia pneumoniae infection and coronary artery disease (CAD). To examine this relationship in Japanese men, serum IgA and IgG antibodies to Chlamydia-specific lipopolysaccharide were measured by enzyme-linked immunosorbent assay in 507 patients with CAD and 200 age-matched controls. CAD patients were divided into (1) 269 patients with myocardial infarction (MI) and (2) 238 patients with chronic coronary heart disease (CCHD). Compared with the control group, the CAD group did not differ in the prevalences of both antibodies (IgA: 23.7 vs 18.0%, p=0.10; IgG: 52.7 vs 51.0%, p=0.6). The index of IgG antibody was not significantly different between CAD and control groups (median 1.19 vs 1.18, p=0.3), whereas the index of IgA antibody was significantly higher in CAD than control group (median 0.60 vs 0.46, p<0.0001). Compared with the control group, the MI group had a significantly higher prevalence of IgA antibody (28.6 vs 18.0%, p=0.007); however, there was no difference in the prevalence of IgG antibody (58.0 vs 51.0%, p=0.13). The CCHD group did not differ in the prevalences of both antibodies (IgA: 18.1 vs 18.0%, p=0.9; IgG: 45.6 vs 51.0%, p=0.2). After the adjustment for coronary risk factors, odds ratios (ORs) of seropositive antibodies for CAD were 1.59 [95% confidence interval (CI): 0.88-2.87, p=0.12] for IgA seropositivity and 0.92 (95%CI: 0.58-1.47, p=0.7) for IgG seropositivity in all cases. In the MI and control groups, ORs of seropositive antibodies for MI were 2.67 (95%CI: 1.32-5.38, p=0.007) for IgA seropositivity, and 1.36 (95%CI: 0.79-2.36, p=0.2) for IgG seropositivity. This study discovered that IgA antibody to Chlamydia was significantly associated with CAD, especially with MI, in Japanese Men and the findings suggest that chronic infection of Chlamydia may be linked to the pathogenesis of MI.
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PMID:Association of seropositivity for antibody to Chlamydia-specific lipopolysaccharide and coronary artery disease in Japanese men. 1126 92

Macrophage immune capability depends on their efficient redox potential expressed in the effective release of reactive oxygen species (ROS) and nitric oxide. In this study the effect of the activation of a specialized Ca(2+) channel on macrophage redox function during Chlamydia pneumoniae infection was explored. C. pneumoniae exhibited a profound and sustained Ca(2+) influx capacity, with evidence of activity attributable to their lipopolysaccharide (cLPS) content. Also the organism showed an additional Ca(2+) influx signal in macrophages exposed to thapsigargin, and there was evidence for the operation of a single ion channel of the L type as demonstrated by the effect of L-type channel antagonists (methoxyverapamil and nimodipine) despite exposure to Ca(2+)-rich medium. C. pneumoniae or cLPS induced intracellular ROS and NO generation in a manner consistent with dependence on intracellular calcium. L-type Ca(2+) channel blocking significantly prompted C. pneumoniae inclusion formation. These findings suggest that Ca(2+) influx signal and redox function in C. pneumoniae-infected macrophages depend on L-type Ca(2+) channel activation.
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PMID:Effective macrophage redox defense against Chlamydia pneumoniae depends on L-type Ca2+ channel activation. 1273 23

Recent studies have suggested that Chlamydia pneumoniae infection is an important factor in the development of atherosclerosis. The C(-260)-->T polymorphism in the CD14 promoter gene has been reported to regulate the density of CD14 expression on monocytes for the activation of monocytes to secrete inflammatory cytokines by lipopolysaccharide. We investigated this genetic marker and its association with C. pneumoniae infection. Among 315 healthy subjects, the distribution of the C(-260)-->T polymorphism in the CD14 promoter gene was 14.9% for the CC genotype, 54.3% for the CT genotype, and 30.8% for the TT genotype. Among subjects with the 3 CD14 genotypes, 59.5%, 64.9%, and 78.3%, respectively, were seropositive for C. pneumoniae. With multiple logistic regression analysis, the odds ratio of C. pneumoniae infection was 2.08 for CD14 TT genotype (95% confidence interval, 1.18-3.69; P=.016). A significant association between the CD14 TT genotype and C. pneumoniae infection was found.
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PMID:Association of CD14 promoter gene polymorphism and Chlamydia pneumoniae infection. 1282 76

Chlamydia pneumoniae infection is associated with atherosclerosis and may be an emerging risk factor in coronary artery disease. C. pneumoniae can infect, multiply within and modulate the function of all atheroma cell types. Specific chlamydial virulence determinants have been identified that permit interaction with host cells and dysregulate cell function. In particular, chlamydial heat shock protein 60 and lipopolysaccharide may modulate cell function to dysregulate lipid metabolism, induce inflammatory cytokine cascades and trigger production of cross-reactive antibodies that initiate and promote atherogenesis. This paper reviews chlamydial heat shock protein 60 and lipopolysaccharide as potential virulence determinants in atherogenesis.
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PMID:Chlamydial heat shock protein 60 and lipopolysaccharide: potential virulence determinants in atherogenesis. 1456 Nov 89

Unregulated uptake of low density lipoprotein (LDL) in macrophages is the hallmark of early atherogenic lesions, and Chlamydia pneumoniae infection of macrophages induces this process by an unknown mechanism. It was therefore aimed in this study to investigate (i) the role of C. pneumoniae in macrophage expression of the lipoprotein lipase (LpL) gene, (ii) the probable role of Ca2+ influx signals and (iii) the effect of the process on LDL uptake. Lipoprotein lipase mRNA expression and LpL activity in infected RAW-264.7 cells were significantly upregulated. A biphasic Ca2+ influx signal was observed in infected cells with a moderate influx (303 nM Ca2+) favoring optimal LpL gene expression. Also, the antagonists of L-type Ca2+ channel in macrophages significantly down-regulated LpL gene expression and the biomolecular content of C. pneumoniae responsible for the observed events was in part found to be Chlamydia lipopolysaccharide (cLPS). Investigations aimed at determining the specific relevance of Ca(2+)-dependent lipoprotein lipase gene expression in C. pneumoniae-infected macrophages showed that the condition caused enhanced uptake of LDL which was abrogated by Calphostin-C-mediated down-regulation of LpL. This discovery of a specialized Ca2+ influx signal-mediated LpL upregulation in C. pneumoniae-infected macrophages provides a mechanistic insight into early events involving C. pneumoniae in macrophage foam cell formation resulting from LDL uptake.
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PMID:Induction of lipoprotein lipase gene expression in Chlamydia pneumoniae-infected macrophages is dependent on Ca2+ signaling events. 1497 48

Several small clinical trials have indicated that antibiotic treatment of Chlamydia pneumoniae infection is associated with a better outcome in patients with coronary artery disease (CAD). It has not been demonstrated whether antibiotic treatment eradicates C. pneumoniae from vascular tissue. The aim of the present study was to assess the effect of clarithromycin on the presence of C. pneumoniae in the vascular tissue of patients with CAD. Patients who had CAD and who were waiting for coronary artery bypass graft surgery were enrolled in a randomized, double-blind, placebo-controlled trial. Patients were treated with clarithromycin at 500 mg or placebo once daily from the day of inclusion in the study until surgery. Several vascular tissue specimens were obtained during surgery. The presence of C. pneumoniae in vascular tissue specimens was examined by immunohistochemical staining (IHC) and two PCR assays. Chlamydia immunoglobulin G (IgG) titers were determined by an enzyme-linked immunosorbent assay at the time of inclusion in the study and 8 weeks after surgery. A total of 76 patients were included, and 180 vascular tissue specimens were obtained (80 specimens from the group treated with clarithromycin and 100 specimens from the group treated with placebo). Thirty-five patients received clarithromycin (mean duration, 27 days; standard deviation [SD], 12.2 days), and 41 patients received placebo (mean duration, 27 days; SD, 13.9 days). IHC detected the C. pneumoniae major outer membrane protein antigen in 73.8% of the specimens from the group treated with clarithromycin and 77.0% of the specimens from the group treated with placebo (P was not significant). Chlamydia lipopolysaccharide antigen was found in only one specimen from the group that received placebo. C. pneumoniae DNA was not detected in any specimen. Baseline Chlamydia-specific IgG titers were equally distributed in both groups and were not significantly different after treatment. There was no indication of an active C. pneumoniae infection in vascular tissue. Chlamydia-specific IgG titers remained unchanged throughout the study in both the antibiotic- and the placebo-treated patients.
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PMID:Effect of clarithromycin treatment on Chlamydia pneumoniae in vascular tissue of patients with coronary artery disease: a randomized, double-blind, placebo-controlled trial. 1575 Jan 3


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