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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of the immune and fibrinolytic systems of the body in 216 patients with different clinical forms of atherosclerosis (exertion and rest stenocardia, arrhythmias, atherosclerotic hypertension), chronic obstructive bronchitis revealed that the antiatherogenous effect of chronic obstructive bronchitis is predetermined on the one side by an increased function of the monocytic-macrophagal link of immunity and on the other by activation of the fibrinolysis system.
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PMID:[The role of the immune and fibrinolytic systems in the inhibition of atherogenesis in chronic obstructive bronchitis]. 144 83

Fibrinolytic system, immune reactivity and isoelectric focusing of serum albumin were examined in 94 patients exhibiting combination of obstructive lung disease (chronic obstructive bronchitis and bronchial asthma) with atherosclerosis. Plasminogen activator showed discrete activity, the discreteness being less in respiratory distress of the I degree but higher in the distress of the II and III degree. Relative number of E-RFC and monocytes expressing receptors to IgM and IgG Fc-fragment decreased. Percentage of EAC-RFC rose. Serum albumin fractions changed pH range due to modification of albumin molecules resultant from forming complexes with fibrinogen degradation products. Concentration of the latter under conditions of respiratory distress induced by obstructive lung diseases associated with atherosclerosis substantially exceeded the standard levels.
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PMID:[Fibrinolysis, immune reactivity and the structure of the blood serum albumin in obstructive lung diseases combined with atherosclerosis]. 207 78

On the basis of a morphological examination of the heart and lungs at 337 autopsies of patients who had died of acute primary myocardial infarction, 108 cases were specified where myocardial infarction was related to a 3-10 year old history of chronic bronchitis. With regard to the bronchopulmonary system, autopsy findings in this series revealed manifestations of bronchitis, pneumosclerosis and emphysema. The myocardial infarction was underlied by stenosing coronary atherosclerosis (89%) in conjunction with thrombosis (76%). A conclusion is drawn as to a more severe course of myocardial infarction in chronic bronchitis patients.
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PMID:[Features of myocardial infarction in chronic bronchitis patients]. 670 Jan 31

There have been established opposite reactions in the cardiovascular system during formation of dust-induced pathology of lungs: a common finding in patients with pneumoconiosis is alterations in the left heart, while in chronic dust bronchitis the same is true of the right heart. In the authors' opinion, different states of pulmonary surfactant in the above conditions account for this observation. Inhibition of synthesis of the pulmonary surfactant associated with the development of the blood and tissue phospholipid deficiency makes for the evolution of atherosclerosis in patients with pneumoconiosis while enhancement of the phospholipid production by the lungs accompanied by elevation of their blood content is an important factor inhibiting the processes of atherogenesis in patients with dust bronchitis.
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PMID:[The role of pulmonary surfactant in the atherogenesis process in patients with dust-induced respiratory organ diseases]. 783 9

Chlamydia are obligate intracellular eubacteria that are phylogenetically separated from other bacterial divisions. C. trachomatis and C. pneumoniae are both pathogens of humans but differ in their tissue tropism and spectrum of diseases. C. pneumoniae is a newly recognized species of Chlamydia that is a natural pathogen of humans, and causes pneumonia and bronchitis. In the United States, approximately 10% of pneumonia cases and 5% of bronchitis cases are attributed to C. pneumoniae infection. Chronic disease may result following respiratory-acquired infection, such as reactive airway disease, adult-onset asthma and potentially lung cancer. In addition, C. pneumoniae infection has been associated with atherosclerosis. C. trachomatis infection causes trachoma, an ocular infection that leads to blindness, and sexually transmitted diseases such as pelvic inflammatory disease, chronic pelvic pain, ectopic pregnancy and epididymitis. Although relatively little is known about C. trachomatis biology, even less is known concerning C. pneumoniae. Comparison of the C. pneumoniae genome with the C. trachomatis genome will provide an understanding of the common biological processes required for infection and survival in mammalian cells. Genomic differences are implicated in the unique properties that differentiate the two species in disease spectrum. Analysis of the 1,230,230-nt C. pneumoniae genome revealed 214 protein-coding sequences not found in C. trachomatis, most without homologues to other known sequences. Prominent comparative findings include expansion of a novel family of 21 sequence-variant outer-membrane proteins, conservation of a type-III secretion virulence system, three serine/threonine protein kinases and a pair of parologous phospholipase-D-like proteins, additional purine and biotin biosynthetic capability, a homologue for aromatic amino acid (tryptophan) hydroxylase and the loss of tryptophan biosynthesis genes.
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PMID:Comparative genomes of Chlamydia pneumoniae and C. trachomatis. 1019 88

Chlamydia pneumoniae is a well-established cause of community-acquired pneumonia and bronchitis in adults and children. Chronic infections with C. pneumoniae have been implicated in the development of atherosclerosis and other diseases in humans. Methods currently used for the culture and propagation of C. pneumoniae are not analogous to the infection as it occurs in vivo. We have established a model of continuous C. pneumoniae infection in vitro. HEp-2 cells inoculated with CM-1 and TW-183 strains have been persistently infected for periods of over 1.5 and 2 years, respectively. The cultures were maintained without centrifugation or the addition of cycloheximide, fresh host cells, or chlamydia. We observed cycles of host cell lysis, detachment, and regrowth with both strains of C. pneumoniae. Continuous C. pneumoniae infections may more closely resemble the actual events as they occur in vivo and, therefore, may be a better model for the in vitro study of C. pneumoniae infection. When we used continuously infected cells to determine the effects of azithromycin and ofloxacin on C. pneumoniae propagation in vitro, we found that both drugs reduced but did not completely eliminate the organism. This may be an important observation, as the failure of antibiotic therapy against C. pneumoniae infection in humans has been described.
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PMID:In vitro activities of azithromycin and ofloxacin against Chlamydia pneumoniae in a continuous-infection model. 1047 77

Chlamydia pneumoniae is a widespread pathogen of humans causing pneumonia and bronchitis. There are many reports of an association between C.PNEUMONIAE: infection and atherosclerosis. We determined the whole genome sequence of C.PNEUMONIAE: strain J138 isolated in Japan in 1994 and compared it with the sequence of strain CWL029 isolated in the USA before 1987. The J138 circular chromosome consists of 1 226 565 nt (40.7% G+C) with 1072 likely protein-coding genes that is 3665 nt shorter than the CWL029 genome. Plasmids, phage- or transposon-like sequences were not identified. The overall genomic organization, gene order and predicted proteomes of the two strains are very similar, suggesting a high level of structural and functional conservation between the two unrelated isolates. The most conspicuous differences in the J138 genome relative to the CWL029 genome are the absence of five DNA segments, ranging in size from 89 to 1649 nt, and the presence of three DNA segments, ranging from 27 to 84 nt. The complex organization of these 'different zones' may be attributable to a unique system of recombination.
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PMID:Comparison of whole genome sequences of Chlamydia pneumoniae J138 from Japan and CWL029 from USA. 1087 62

In the past decade there has been renewed interest in the old hypothesis that infections increase the risk of developing cardiovascular disease and stroke. There is now a convincing body of evidence that atherosclerosis has a major inflammatory component and is much more than the simple vascular accumulation of lipids. Infectious agents that have been linked to an increased risk of coronary heart disease (CHD) include Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpesviruses. The concept has emerged that each of these agents is an independent risk factor for CHD and that common chronic infections are important. In addition, periodontal infections have also been implicated as one of several factors contributing to the development of CHD. Evidence supporting a causative role of chronic infections in CHD is largely circumstantial. However, the evidence is sufficiently strong to warrant further examination of the possible link between chronic infections and CHD. In this review the lines of evidence for a causative role of C. pneumoniae in the development of CHD are summarized and contrasted with the lines of evidence suggesting a periodontal infection--CHD association. If common or widespread chronic infections are truly important risk factors for CHD, it is unlikely that a single infection will be shown to be causative. It is likely that the entire microbial burden of the patient from several simultaneous chronic infections is more important (e.g., H. pylori-caused gastric ulcers + C. pneumoniae-caused bronchitis + periodontitis). Increased cooperation between cardiologists and periodontists will be required to determine if, and what, combinations of common chronic infections are important in the pathogenesis of CHD and stroke.
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PMID:Periodontal infections and cardiovascular disease--how strong is the association? 1135 66

Chlamydia pneumoniae causes a range of respiratory infections including bronchitis, pharyngitis and pneumonia. Infection has also been implicated in exacerbation/initiation of asthma and chronic obstructive pulmonary disease (COPD) and may play a role in atherosclerosis and Alzheimer's disease. We have used a mouse model of Chlamydia respiratory infection to determine the effectiveness of intranasal (IN) and transcutaneous immunization (TCI) to prevent Chlamydia lung infection. Female BALB/c mice were immunized with chlamydial major outer membrane protein (MOMP) mixed with cholera toxin and CpG oligodeoxynucleotide adjuvants by either the IN or TCI routes. Serum and bronchoalveolar lavage (BAL) were collected for antibody analysis. Mononuclear cells from lung-draining lymph nodes were stimulated in vitro with MOMP and cytokine mRNA production determined by real time PCR. Animals were challenged with live Chlamydia and weighed daily following challenge. At day 10 (the peak of infection) animals were sacrificed and the numbers of recoverable Chlamydia in lungs determined by real time PCR. MOMP-specific antibody-secreting cells in lung tissues were also determined at day 10 post-infection. Both IN and TCI protected animals against weight loss compared to non-immunized controls with both immunized groups gaining weight by day 10-post challenge while controls had lost 6% of body weight. Both immunization protocols induced MOMP-specific IgG in serum and BAL while only IN immunization induced MOMP-specific IgA in BAL. Both immunization routes resulted in high numbers of MOMP-specific antibody-secreting cells in lung tissues (IN>TCI). Following in vitro re-stimulation of lung-draining lymph node cells with MOMP; IFNgamma mRNA increased 20-fold in cells from IN immunized animals (compared to non-immunized controls) while IFNgamma levels increased 6- to 7-fold in TCI animals. Ten days post challenge non-immunized animals had >7,000 IFU in their lungs, IN immunized animals <50 IFU and TCI immunized animals <1,500 IFU. Thus, both intranasal and transcutaneous immunization protected mice against respiratory challenge with Chlamydia. The best protection was obtained following IN immunization and correlated with IFNgamma production by mononuclear cells in lung-draining LN and MOMP-specific IgA in BAL.
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PMID:Comparison of intranasal and transcutaneous immunization for induction of protective immunity against Chlamydia muridarum respiratory tract infection. 1615 55

The article deals with brain blood flow autoregulation evaluated through transcranial Doppler study in dust bronchitis patients with early cerebral atherosclerosis in dependence on presence or absence of respiratory failure. Present respiratory failure in these patients causes additional disorders in brain blood flow autoregulation, especially during a stage of early signs of brain circulation insufficiency.
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PMID:[Autoregulation of brain blood flow in dust bronchitis patients with early cerebral atherosclerosis]. 1681 98


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