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Query: UMLS:C0032285 (
pneumonia
)
54,520
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Reactive oxygen intermediates (ROI) such as superoxide (O2-), hydrogen peroxide (H2O2) and hydroxyl radicals (.OH) are involved in the pathogenicity of various diseases. There is also evidence that superoxide is involved in disease progression following infection by influenza virus, HIV-1 and human cytomegalovirus (HCMV). Healthy donor-derived peripheral blood monocytes/macrophages, which seem to be the major reservoir for HCMV in vivo, showed significantly higher generation of O2- after HCMV infection. The importance of O2- in cytomegalovirus
pneumonitis
was also supported in a mouse model system using mouse cytomegalovirus. In addition, the importance of HCMV-induced ROI was also shown in the restenosis and
atherosclerosis
of smooth muscle cells. This review highlights the relationship between HCMV infection and ROI.
...
PMID:[Superoxide generation and human cytomegalovirus infection]. 946 68
In the last years several new data allow a controversial but convincing interpretation of the pathogenesis of
atherosclerosis
(arteriosclerosis).
Atherosclerosis
can be apparently the result of ultrachronic persistent infection by Chlamydia pneumoniae and not the result of different risk factors. The main arguments for the chlamydial genesis are: 1. Correlation of coronary heart disease and other atherosclerotic disease with antibodies against C. pneumoniae. 2. C. pneumoniae could be detected with different techniques (PCR, immunohistology, electromicroscopy, culture) in a high percentage in atheromas from different sites. 3. Three international studies with macrolides in coronary heart disease were successful. 4. The target cells of
atherosclerosis
(endothelia, macrophages, muscle cells) can be infected by C. pneumoniae in vitro. 5. Positive animal experiments. The Koch-Henle criteria for the proof of the etiology are largely fulfilled--even if there are doubts about the validity of these criteria in chronic local infections. A number of unexplainable aspect of
atherosclerosis
can be seen in a new light. The higher incidence of coronary heart disease in young males has a parallel in the remarkable androtropism of many bacterial diseases (pneumococcal
pneumonia
, tuberculosis). The reduction of incidence of atherosclerotic diseases since 1965 can be explained by the much higher intake of doxycyclin and macrolides. The low incidence of coronary heart disease in France--sometimes regarded as an effect of red wine--can be explained as a result of a much higher use of antichlamydial antibiotics. The increase of inflammatory parameters (C-reactive protein, fibrinogen, leucocytes) before acute coronary infarction are not risk factors but signs of an active chronic infection. The interpretation is possible, that atherogenic changes in lipids like increase of LDL and decrease of HDL are not risk factors but consequence of chronic arterial infection by chlamydia. The low incidence of
atherosclerosis
in the tropics--despite high frequency of chlamydial infection--is difficult to explain. Vascular infection can be related with the age of the patient at the primary infection. With low hygiene, intestinal primary infections in early childhood can be possible. Arterial infection would be thus a result of a primary infection in adolescence ("yet another poliomyelitis story"). There are good arguments for the thesis that C. pneumoniae is the primary cause of
atherosclerosis
and not a secondary invader. The consequence, nevertheless, is similar: Antibiotics get a key role. The macrolides roxithromycin, azithromycin, clarithromycin and the tetracyclin doxycyclin fulfill the criteria as potential antichlamydial agents. In general a longer treatment (6 to 8 to 12 weeks) seems advisable. It is necessary to start international studies with antibiotics in coronary infarction and other clinical manifestations of
atherosclerosis
. The relevant antibiotics licensed for chlamydial infections are cheap and safe. Despite of the urgent need for controlled studies, it seems already justified to treat high-risk patients with antibiotics. Meticulous protocols and long-term control of patients are necessary to evaluate the therapeutic effects. Preventive studies in patients without clinical manifestation of
atherosclerosis
are urgently needed. The risks of resistance or side effects are neglectable, but the organisation of such studies would be very difficult.
...
PMID:[Arteriosclerosis as a sequela of chronic Chlamydia pneumoniae infection]. 964
Animal models are used extensively in the ongoing investigation of a possible causal link between Chlamydia pneumoniae infection and conditions such as asthma and cardiovascular disease. Respiratory infections have been studied in monkeys, while mouse and rabbit models have been used to study both respiratory and cardiovascular infections. The degree of disease induced in mice depends on the strain used, the virulence of the C. pneumoniae strain used, and the dose administered. A characteristic mononuclear
pneumonitis
occurs, although the infection is systemic and the agent is found outside the lungs, in the circulation, spleen and liver. The infective dose used in the model tends to produce persistent infection, with inflammation continuing after the agent can no longer be cultured from the lungs. In reinfected animals the titre of infective chlamydia in lungs is much diminished, but the inflammation can be quite marked. The continuous persistence of the agent can be demonstrated by polymerase chain reaction (PCR), or, in chronically infected animals, after immunosuppression with cortisone. New Zealand White (NZW) rabbits provide an experimental model, not only for lung infections, but also for C. pneumoniae-induced
atherosclerosis
. Three laboratories have now reported that after inoculation, plaques develop in the arterial walls of experimental animals on a normal diet. In addition, one laboratory has reported from their studies on
atherosclerosis
in apoE-deficient and normal mice, that the persistence of the agent in aortic walls could be seen. Further studies are needed to evaluate the effect of the strain of chlamydia and dosage used, the importance of reinfection, the effect of diet and the effect of antibiotic treatment in these models.
Atherosclerosis
1998 Oct
PMID:Animal models for Chlamydia pneumoniae infection. 985 20
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.
...
PMID:Comparative genomes of Chlamydia pneumoniae and C. trachomatis. 1019 88
Common complications of cardiac transplantation include infection, rejection, accelerated coronary artery
atherosclerosis
, and lymphoproliferative disease. The authors reviewed radiographic and computed tomographic (CT) features of cardiac transplantation and its complications in a series of 232 patients (with 89 complications and 49 deaths). Normal postoperative findings in the first few weeks after surgery included enlarged cardiac silhouette, pneumomediastinum, pneumothorax, pneumopericardium, subcutaneous emphysema, and mediastinal widening. Infection was the most common complication, with
pneumonia
being the leading infectious condition (28 cases, with Aspergillus [n = 11] and cytomegalovirus [n = 10] being the most common pathogens) and the cause of death in seven cases. Although many cases of pulmonary infections occur in the first 3-4 months after surgery, in this series several cases developed up to 3 years afterward. Radiographic signs of acute rejection were nonspecific in the eight patients affected who died, and endomyocardial biopsy was used to confirm the suspected diagnosis. Accelerated
atherosclerosis
occurred in 13 patients between 10 months and 6.5 years after transplantation and led to death in eight. Lymphoproliferative disorders, which range from benign lymphoid hyperplasia to malignant lymphoma and which are the third leading cause of death beyond the immediate perioperative period in heart transplant recipients, developed in four patients who later died. Other complications related to endomyocardial biopsy and cardiothoracic surgery (i.e., pneumothorax, hemothorax, pneumomediastinum, mediastinitis, aortic dissection, aortic pseudoaneurysm, and pulmonary embolism) occurred in 31 cases and were diagnosed with radiography and CT.
...
PMID:Imaging of cardiac transplantation complications. 1019 82
Rural health care delivery is often inferior to that of urban areas. Although health services do not have to be identical in the two settings, quality services appropriate for the needs of rural communities are imperative. Moreover, health education and promotion should be seen as an immediate and viable strategy for (a) reducing risk factors and health care needs, and (b) increasing the cost effectiveness of existing services. The appropriateness and prioritization of health care services and health education/promotion can only be realized if health professionals are aware of rural versus urban needs. To facilitate our knowledge of such differences, the mortality rates of the 10 leading causes of death were compared for each county in Ohio and differences between rural and urban mortality were analyzed. Counties were categorized according to "density" (persons per square mile) and "percent urban" (percent of county area classified as urban). The analysis demonstrated that there were no significant differences between rural and urban counties in mortality due to cancer, pulmonary disease, diabetes mellitus,
atherosclerosis
, and suicide. Mortality related to cardiovascular disease, cerebrovascular disease, accidents, and influenza/
pneumonia
was significantly higher in rural counties, while deaths due to chronic liver disease were significantly greater in urban counties.
...
PMID:Difference in rural and urban mortality: implications for health education and promotion. 1029 26
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.
...
PMID:[Chlamydia pneumoniae pneumonia]. 1042 Sep 52
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.
...
PMID:In vitro activities of azithromycin and ofloxacin against Chlamydia pneumoniae in a continuous-infection model. 1047 77
The strength of the epidemiologic and clinical associations of Chlamydia pneumoniae with
atherosclerosis
can be increased by the demonstration that C pneumoniae can initiate and sustain growth in human vascular cells as well as in animal models. To investigate the biological basis for the dissemination and proliferation of this organism in vascular cells, the in vitro growth of C pneumoniae was studied in 2 macrophage cell lines, peripheral blood monocyte (PBMC)-derived macrophages, human bronchoalveolar lavage (BAL) macrophages, several endothelial cell lines, and aortic artery smooth muscle cells. Five of 5 strains of C pneumoniae were capable of 3 passages in human U-937 macrophages and in murine RAW 246.7 macrophages. Titers were suppressed in both macrophage types with each passage as compared with growth in HEp-2 cells. Both human BAL macrophages and PBMC-derived macrophages were able to inhibit C
pneumonia
eafter 96 hours' growth. Eleven C pneumoniae strains were capable of replicating in normal human aortic artery-derived endothelial cells, umbilical vein-derived endothelial cells, and pulmonary artery endothelial cells. Infection in human aortic artery smooth muscle cells was also established for 13 strains of C pneumoniae. C pneumoniae was also capable of growing in endothelial cells derived from human cadaver coronary artery endothelial cells (CAEC). U-937 human macrophages that were infected with C pneumoniae were capable of transmitting the infection to CAEC when they were brought into contact with the endothelial cells by centrifugation, rocking overnight, and direct layering overnight, with and without using artificial laboratory tissue culture enhancements, such as centrifugation of the inoculum and cycloheximide in the growth media. The in vitro ability of C pneumoniae to maintain infections in macrophages, endothelial cells, and aortic smooth muscle cells may provide support for the hypothesis that C pneumoniae can infect such cells, which when followed by an immune response may contribute to atheroma formation in vivo. Stimulation of cytokine responses by infection with C pneumoniae has indicated that this organism is capable of interacting with the immune system. In vitro infection by C pneumoniae of U-937 macrophages stimulated the production of IL-1beta, IFN-gamma, and TNF-alpha in tissue culture. Human CAEC that are infected with C pneumoniae produce more IL-8 compared with those inoculated with killed C pneumoniae or negative control cells, indicating a chemokine response to infection that may play a role in recruitment of inflammatory cells to sites of infection in vascular cells. When IFN-gamma was used to up regulate HEp-2 and U-937 cells before infection by C pneumoniae, inhibition of a lytic growth cycle occurred in a dose related response. However, removal of the IFN-gamma after 24 to 48 hours' exposure allowed subsequent productive growth in the cells, perhaps indicating the prior induction of a persistent infection. More studies are needed to study the complex relationship between lytic infection and persistence, the ability of C pneumoniae to affect the immune response of vascular cells, and the potential for C pneumoniae to influence the initiation of or progression of atheromatous lesions.
...
PMID:In vitro infection and pathogenesis of Chlamydia pneumoniae in endovascular cells. 1053 60
Chlamydia pneumoniae is strongly implicated in the pathogenesis of
atherosclerosis
in human beings. Animal models are important to help establish causality, to understand the mechanism of infection induced atherogenesis, to examine interaction of other factors or variables, to explore treatment regimens and their efficacy, and to help develop a vaccine for prevention. To date, the rabbit model is the only animal model shown to develop de novo atherosclerotic changes with C pneumoniae infection. However, the mouse model may be useful to show enhancement with other factors such as hypercholesterolemia and to explore pathogenic mechanisms. In our studies, we have shown that C pneumoniae respiratory infection in the rabbit results in early atherosclerotic changes in 26% with single inoculation and in 35% after triple inoculation, but sham infection or infection with Mycoplasma pneumoniae does not result in similar changes. Early treatment (5 days after inoculation) with 30 mg/kg per day azithromycin once every 6 days was 87% effective in preventing atherosclerotic changes, but delayed treatment (6 weeks after inoculation) was ineffective. Further studies are needed with longer or more aggressive regimens or possible combination of agents to determine whether it is possible to reverse preformed lesions. An effective vaccine for prevention of C pneumoniae -induced
pneumonia
and possibly atherosclerotic lesions in human beings would have tremendous application and would circumvent the shortcomings of antibiotic therapy.
...
PMID:Value of animal models for Chlamydia pneumoniae-related atherosclerosis. 1053 61
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