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Biomedical subjects

M Maass

Publications and source records attributed to M Maass.

At least 37 records · Page 2Linked to original sources
PubMed2001

Association between infection with Helicobacter pylori and Chlamydia pneumoniae and risk of ischemic stroke subtypes: Results from a population-based case-control study.

BACKGROUND AND PURPOSE: Helicobacter pylori and Chlamydia pneumoniae have been associated epidemiologically and pathogenetically with coronary atherosclerosis. However, population-based data on chronic infection and stroke are lacking. Therefore, we investigated the association of both bacterial pathogens and ischemic stroke subtypes in a population-based case-control study. METHODS: Patients with first ischemic stroke in the population-based Erlangen Stroke Project were collected as cases. Neighborhood controls were drawn from the study population, matched for age, sex, and place of residence. IgG antibodies to H pylori were measured by enzyme immunoassay, and IgG antibodies to C pneumoniae were measured by microimmunofluorescence technique. Conditional logistic regression was used. Analyses were stratified for etiologic stroke subtypes according to Trial of Org 10172 in Acute Stroke Treatment (TOAST) criteria. RESULTS: A total of 145 case and 260 control subjects were included. Chronic H pylori infection was associated with a higher risk of stroke caused by small-artery occlusion (adjusted odds ratio, 3.31; 95% CI, 1.15 to 9.56) and a lower risk of cardioembolic stroke (adjusted odds ratio, 0.21; 95% CI, 0.06 to 0.71). Overall, elevated H pylori as well as elevated C pneumoniae antibodies were not associated with ischemic stroke. CONCLUSIONS: Our population-based study does not provide evidence of any strong association between the immune response to C pneumoniae as a marker of prior infection and ischemic stroke. Further studies are required to reveal the role of chronic H pylori infection as an independent risk factor for the subgroup small-artery occlusion.

Aged↗
PubMed2001

Presence of Chlamydia pneumoniae DNA in the cerebral spinal fluid is a common phenomenon in a variety of neurological diseases and not restricted to multiple sclerosis.

Chlamydial DNA and viable organisms have been reported in the cerebrospinal fluid (CSF) of multiple sclerosis (MS) patients. We investigated whether this phenomenon is specific for MS and not occurring in patients with other neurological diseases (OND) or in healthy controls and whether it is caused by infected blood monocytes having crossed the blood-brain barrier. Twelve (21%) of fifty-eight MS patients and 20 (43%) of 47 OND patients had Chlamydia pneumoniae DNA in the CSF as determined by nested polymerase chain reaction. Viable organisms were cultured from one OND patient. We failed to detect C. pneumoniae in the CSF of 67 neurologically healthy persons. C. pneumoniae was detected in parallel in the blood monocytes of 2 of 6 CSF-positive MS patients and in 8 of 10 CSF-positive OND patients. Thus, chlamydial presence cannot exclusively be explained as being caused by contaminating infected monocytes that have crossed the blood-brain barrier. In peripheral blood mononuclear cell-negative patients, chlamydia have been cleared from the circulation but persist in the central nervous system (CNS), indicating the establishment of a chronic process. In summary, the presence of C. pneumoniae in patients with neurological diseases is a common phenomenon and is not restricted to MS patients. The pathogenetic relevance of a chronic chlamydial CNS infection for neurological diseases remains unclear, but the hypothesis that susceptible patients may be impaired in their ability to clear chlamydiae from the CNS requires further examination.

Adolescent↗
PubMed2001

[Infection hypothesis of coronary heart disease].

It is well accepted that coronary artery disease is linked to an inflammatory process. It is unproven however whether either infectious agents may cause or accelerate coronary artery disease or the inflammatory process is due to metabolic or toxic effects. Among the possible infectious agents Chlamydia pneumoniae is the most likely bacterium involved in atherosclerosis. The arguments in favour of Chlamydia pneumoniae originate from seroepidemiologic studies and from detection and isolation of bacteria from vascular lesions. This review summarises the present understanding of the role of bacterial infection for development or progression of coronary artery disease.

Animals↗
PubMed2000

Hydroxymethylglutaryl coenzyme A reductase inhibitors modify the inflammatory response of human macrophages and endothelial cells infected with Chlamydia pneumoniae.

BACKGROUND: In patients with atherosclerosis, hepatic hydroxymethylglutaryl coenzyme A reductase (CSE) inhibitors may reduce the activation of inflammation. Because Chlamydia pneumoniae infection has been linked to coronary artery disease through the induction of plaque inflammation, we investigated whether cerivastatin affects the infection rate of human macrophages and endothelial cells (ECs) and their proinflammatory activation after chlamydial infection. METHODS AND RESULTS: Macrophages were collected from the alveolar compartment of 6 volunteers and 10 patients with chronic bronchitis. ECs were obtained from 10 umbilical cords. The C. pneumoniae strain CWL was incubated with macrophages or ECs in the presence and absence of the CSE inhibitor cerivastatin. The infection rate was determined by immunofluorescence microscopy. The release of monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), and tumor necrosis factor (TNF)-alpha was quantified by ELISA. The release of oxygen radicals was determined by ferricytochrome assay. Infection rates were tendentially lower after the preincubation of macrophages with CSE inhibitors (17.2% versus 9. 3% and 18.2% versus 10.4%, respectively; P=NS). The secretion of MCP-1, IL-8, and TNF-alpha by infected macrophages from volunteers increased. Coincubation with cerivastatin resulted in significantly lower MCP-1 and IL-8 production, whereas the release of TNF-alpha remained unaffected. Similar effects regarding chemokine release were observed in ECs. CONCLUSIONS: CSE inhibitors modify the inflammatory response of human immune cells to C. pneumoniae. This finding could be relevant for the therapeutic potential of CSE statins in patients with atherosclerosis and C. pneumoniae infection.

Adult↗
PubMed2000

Association of serology with the endovascular presence of Chlamydia pneumoniae and cytomegalovirus in coronary artery and vein graft disease.

BACKGROUND: Chemotherapeutic treatment for patients with symptomatic coronary artery disease to reduce cardiovascular events may be initiated in response to elevated antibody titers against Chlamydia pneumoniae or cytomegalovirus. How antibody titers are associated with the endovascular presence of these microorganisms is still unclear. METHODS AND RESULTS: Antibody titers against C pneumoniae (microimmunofluorescence) and cytomegalovirus (ELISA) in patients undergoing primary (coronary desobliterates, n=80) or repeated CABG (occluded vein grafts, n=45) were correlated with the endovascular presence of the 2 microorganisms. C pneumoniae was detected by means of a nested polymerase chain reaction (PCR) and by culturing. Both conventional PCR and quantitative PCR were applied for detection of cytomegalovirus. C pneumoniae (PCR/culture) was detected in 19/9% (15/80 and 7/80) of coronary desobliterates and in 18/11% (8/45 and 5/45) of occluded vein grafts. There was no statistical evidence that IgG values differed between patients with or without C pneumoniae detection who were undergoing primary CABG. In contrast, repeated-CABG patients with a positive PCR (P=0.0027) or C pneumoniae culture (P=0.0018) had distinctly elevated IgG titers compared with patients in whom C pneumoniae was not detected. Cytomegalovirus could not be detected in the examined specimens. CONCLUSIONS: Cytomegalovirus infection does not seem to be associated with advanced coronary artery lesions. C pneumoniae antibody titers are not associated with the endovascular presence of C pneumoniae in patients with coronary artery disease. The observed strong association between elevated IgG titers and the detection of C pneumoniae in occluded vein grafts warrants further investigation.

Aged↗
PubMed2000

Atherogenetically relevant cells support continuous growth of Chlamydia pneumoniae.

The obligate intracellular bacterium Chlamydia pneumoniae has been implicated in the pathogenesis of atherosclerosis since viable pathogen has been recovered from plaques. Chlamydiae are epithelial pathogens notorious for causing persistent infection. Atherosclerosis, however, is a chronic inflammatory disease involving mesenchymal cells of the vascular wall. A bacterial contribution to atherosclerosis appears more relevant if the resident mesenchymal cells of the vascular wall that constitute the plaque can support chlamydial infection continuously. Therefore we inoculated immortalized and primary mesenchymal cells with a vascular and a respiratory Chlamydia pneumoniae isolate. Primary human coronary artery endothelial and smooth muscle cells, primary human embryonic fibroblasts as well as the immortalized cell lines were permissive for continuous growth of both strains. Thus, the resident vascular cells that produce the atheromatous plaque can acquire permanent productive. Chlamydia pneumoniae infection. Immortalized monocytic cells and peripheral blood monocytes also supported chlamydial growth, though productive infection ceased after 5 passages. Monocytes/macrophages are not resident cells of the vascular wall but have an active role in plaque formation. Systemic circulation and transendothelial migration makes them a potential vector system for chlamydial distribution. These findings add further plausibility to the hypothesis of a chronic infectious component in the multifactorial condition of atherosclerosis. Further studies must precisely define chlamydial target cells in vivo and differentiate infection in resident cells of the vascular wall from a presence limited to migrating macrophages. Endovascular infection might provide an explanation for unclear phenomena of atherogenesis like mesenchymal cell proliferation and its distinct inflammatory component.

Arteriosclerosis↗
PubMed2000

Detection of Chlamydia pneumoniae within peripheral blood monocytes of patients with unstable angina or myocardial infarction.

Because individual diagnoses of vascular infection with Chlamydia pneumoniae depend entirely on surgically removed tissues, a better assay to predict vascular infection is needed. Polymerase chain reaction detection of chlamydial DNA was applied to CD14-positive cells collected from 238 patients with angiographically identified unstable angina or acute myocardial infarction. C. pneumoniae was detected in 52 (28%) of 188 persons with unstable angina and in 13 (26%) of 50 persons with myocardial infarction. Differences between groups were not significant. C. pneumoniae is present in monocytes/macrophages of a significant proportion of persons with progressive coronary artery disease. Infarction is not accompanied by a rise in chlamydial detection rates. The potential role of chlamydiae in coronary atherosclerosis may therefore be more related to acceleration of disease or systemic effects by persistent infection than to sudden initiation of infarction by acute infection.

Adult↗
PubMed2000

Cardiovascular infection by Chlamydia pneumoniae is not related to apolipoprotein E genotype.

Chlamydia pneumoniae is detectable in the blood vessels of patients suffering from arteriosclerosis. Risk for arteriosclerosis is modulated by the apolipoprotein E (apoE) allele. We assessed the significance of the apoE genotype as a risk factor for vascular C. pneumoniae infection by determining the genotype of 30 coronary heart disease patients with PCR-proven C. pneumoniae infection of coronary artery tissue. The apoE genotype is not distinctly associated with an increased risk for vascular C. pneumoniae infection.

Apolipoproteins E↗
PubMed2000

Failure to detect Chlamydia pneumoniae in brain sections of Alzheimer's disease patients.

A recent North American study detected Chlamydia pneumoniae in 17 of 19 brains of Alzheimer's patients and supposed a C. pneumoniae infection to be a risk factor for Alzheimer's disease (AD). In this study, we analyzed paraffin-embedded tissue samples of 20 AD patients by nested PCR and immunocytochemistry with a panel of antichlamydial antibodies and could detect neither C. pneumoniae-specific DNA nor chlamydial antigens. From our data, the presence of C. pneumoniae in the brains of Alzheimer's patients is not a common phenomenon; an association remains questionable.

Aged↗
PubMed2000

Transportation savings and medical benefits of a teleneuroradiological network.

Since 1996, Turku University Central Hospital has offered teleradiology consultations regarding computerized tomography examinations of the brain to three regional hospitals in Finland, in which neurosurgical or neuroradiological specialist services are not available, in order to avoid unnecessary patient transportation. We performed a retrospective survey of the teleconsultations performed in 1998. Medical records and the relevant radiology images were obtained. During the study period, teleconsultations were carried out for a total of 83 patients, of whom 16 were transported to the university hospital (i.e. 81% of these patients had avoided unnecessary transportation). The total savings amounted to 42,100 ECU. Of the 16 transported patients, 12 were immediately operated on in the university hospital. It was judged that, because of the consultation service, the patients undergoing an operation had benefited from a more rapid and a more complete recovery. In 1998 the teleradiology consultation service was established as part of the routine work of the Medical Imaging Centre and a fee for its services was adopted.

Adolescent↗
PubMed1999

Chlamydia pneumoniae infection of vascular smooth muscle and endothelial cells activates NF-kappaB and induces tissue factor and PAI-1 expression: a potential link to accelerated arteriosclerosis.

BACKGROUND: Recent reports link C. pneumoniae infection of arteriosclerotic lesions to the precipitation of acute coronary syndromes, which also feature tissue factor and plasminogen activator inhibitor 1 (PAI-1) overexpression. We investigated whether or not C. pneumoniae can induce thrombogenicity by upregulation of procoagulant proteins. METHODS AND RESULTS: Human vascular endothelial and smooth muscle cells were infected with a strain of C. pneumoniae isolated from an arteriosclerotic coronary artery. Tissue factor, PAI-1, and interleukin-6 expression was increased in infected cells. Concomitantly, NF-kappaB was activated and IkappaBalpha degraded. p50/p65 heterodimers were identified as the components responsible for the NF-kappaB activity. CONCLUSIONS: These data provide evidence that C. pneumoniae infection can induce procoagulant protein and proinflammatory cytokine expression. This cellular response is accompanied by activation of NF-kappaB. Our results demonstrate how C. pneumoniae infection may initiate acute coronary syndromes.

Arteriosclerosis↗
PubMed1999

Detection of Chlamydia pneumoniae but not cytomegalovirus in occluded saphenous vein coronary artery bypass grafts.

BACKGROUND: A causal relation between atherosclerosis and chronic infection with Chlamydia pneumoniae and/or cytomegalovirus (CMV) has been suggested. Whether the unresolved problem of venous coronary artery bypass graft occlusion is related to infection with C pneumoniae and/or CMV has not been addressed. METHODS AND RESULTS: Thirty-eight occluded coronary artery vein grafts and 20 native saphenous veins were examined. Detection of C pneumoniae DNA was performed by use of nested polymerase chain reaction (PCR). Homogenisates from the specimen were cultured for identification of viable C pneumoniae. Both conventional PCR and quantitative PCR for detection of CMV DNA were applied. Differential pathological changes (degree of inflammation, smooth muscle cell proliferation [MIB-1]) were determined and correlated to the detection of both microorganisms. C pneumoniae DNA could be detected in 25% of occluded vein grafts. Viable C pneumoniae was recovered from 16% of occluded vein grafts. Except for 1 native saphenous vein, all control vessels were negative for both C pneumoniae detection and culture. All pathological and control specimens were negative for CMV DNA detection. Pathological changes did not correlate with C pneumoniae detection. CONCLUSIONS: Occluded aorto-coronary venous grafts harbor C pneumoniae but not CMV. The detection of C pneumoniae in occluded vein grafts warrants further investigation.

Adult↗
PubMed1999

Systemic infection of an immunocompromised patient with Methylobacterium zatmanii.

We describe the identification of Methylobacterium zatmanii as the causative agent of bacteremia and fever in an immunocompromised patient. The patient, a 60-year-old man, had a 5-month history of acute myeloid leukemia and had been on chemotherapy throughout this period. Seven days after the onset of neutropenia, the patient developed fever. The combination of ciprofloxacin, co-trimoxazole, imipenem, amikacin, and vancomycin led to a complete defervescence. On subculture from six positive blood cultures, the organism grew only on buffered charcoal yeast extract agar and not on standard agars. Identification by universal PCR and subsequent sequence analysis of the amplified 16S rRNA gene segment was achieved. This identification by molecular biology techniques was confirmed by conventional biochemical tests. To our knowledge, this is the first description of M. zatmanii isolated from patient material.

Acute Disease↗
PubMed1998

Endovascular presence of viable Chlamydia pneumoniae is a common phenomenon in coronary artery disease.

OBJECTIVES: We sought to examine coronary arteries for the presence of viable bacteria of the fastidious species Chlamydia pneumoniae. BACKGROUND: The respiratory pathogen C. pneumoniae has been implicated in the pathogenesis of coronary artery disease (CAD). Previous studies have demonstrated an antichlamydial seroresponse to be a cardiovascular risk factor and coronary atheromata to contain chlamydial components in varying proportions. Endovascular demonstration of replicating bacteria is required to provide evidence for an infectious component in CAD and a rationale to discuss antimicrobial therapy. METHODS: Myocardial revascularization was performed in 70 patients. Atherosclerotic lesions from 53 coronary endarterectomy and 17 restenotic bypass samples were cultured and subjected to nested polymerase chain reaction (PCR) for C. pneumoniae. Antichlamydial immunoglobulin G (IgG), IgA and IgM was examined by microimmunofluorescence. RESULTS: Viable C. pneumoniae was recovered from 11 (16%) of 70 atheromata, and chlamydial deoxyribonucleic acid (DNA) was detected in 21 (30%) of 70 atheromata; 17 nonatherosclerotic control samples were PCR-negative (p < 0.01). Fifteen (28%) of 53 endarterectomy and 6 (35%) of 17 bypass samples were PCR-positive. DNA sequencing of six different PCR products did not reveal differences between coronary isolates and respiratory reference strains, suggesting that common respiratory strains gain access to the systemic circulation. Serologic results did not correlate with direct detection results and did not identify individual endovascular infection. CONCLUSIONS: A significant proportion of atherosclerotic coronary arteries harbor viable C. pneumoniae. This finding supports the hypothesis of a chlamydial contribution to atherogenesis. Whether chlamydiae initiate atherosclerotic injury, facilitate its progression or colonize atheromata is unknown. However, the endovascular presence of viable bacteria justifies a controlled clinical investigation of antimicrobial treatment benefit in the therapy and prevention of CAD.

Adult↗
PubMed1998

[Persistence of Chlamydia pneumoniae in human arteriosclerotic plaque substance. Evidence and consequences].

The obligate intracellular bacterium Chlamydia pneumoniae has recently been implicated in the pathogenesis of atherosclerosis. Serological response to Chlamydia pneumoniae statistically indicates an increased risk of coronary artery disease and myocardial infarction. This surprising relation is corroborated by the presence of chlamydial structures and even viable Chlamydia pneumoniae in atherosclerotic plaques. These findings have already resulted in initial studies on the potential benefit of antimicrobial therapy in coronary heart disease. However, experimental proof of an etiological role of Chlamydia pneumoniae in arteriosclerosis has not yet been accomplished since a well established animal model and a system of genetic recombination are not yet available. In addition, clinical evaluation of patients is complicated by the lack of a useful parameter to indicate the risk of endovascular infection. Whether chlamydiae initiate atherosclerotic injury. facilitate progression of existing plaques, or merely colonize the lesions is therefore not known. Chlamydial contribution to the development of atherosclerosis is a fascinating hypothesis that may initiate a radical change of clinical practice for one of the leading causes of death. At the current state of scientific knowledge, however, an experimental antichlamydial treatment in coronary heart disease may only be justified in well controlled clinical trials.

Arteriosclerosis↗