Chlamydia pneumoniae DNA in Peripheral Venous Blood Samples from Patients with Carotid Artery Stenosis

Freidank, Heike; Lux, Árpád; Dern, Peter; Meyer‐König, Ursula; Els, T

doi:10.1007/s10096-001-0647-3

Cited by 14 publications

(11 citation statements)

References 15 publications

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“…Many additional patients returned for 11 visit during the study period to have a blood sample obtained, and none had detectable C. pneumoniae nucleic acid in PBMCs (data not shown). As summarized in table 4, our uniformly negative results are in contrast with the wide range of prevalence in 18 similar published controlled studies [4,[24][25][26][27][28].…”

Section: Discussioncontrasting

confidence: 85%

“…The definition of a positive PCR result is not provided in 8 of the 18 published controlled studies [4,24,26,28]. The other 10 studies used highly variable definitions of a positive result [4,25,27]; it appears that any single determination of positivity was considered to be a positive result in most of these studies [4,25]. Of interest, if we had accepted a positive result in only 1 of the replicate aliquots, then the prevalence of positivity among case patients and control subjects would have been 8.8% and 10.5%, respectively.…”

Section: Discussionmentioning

confidence: 96%

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Detection of CirculatingChlamydophila pneumoniaein Patients with Coronary Artery Disease and Healthy Control Subjects

et al. 2009

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Section: Discussioncontrasting

confidence: 85%

Section: Discussionmentioning

confidence: 96%

Detection of CirculatingChlamydophila pneumoniaein Patients with Coronary Artery Disease and Healthy Control Subjects

et al. 2009

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“…They found that testing 1, 3, or 5 replicates detected 3, 5, or 9 of 10 true C. pneumoniae DNA-positive PBMC samples. With this in mind, and being well-aware of the pitfalls of conventional PCR, it is not astonishing that others 14,15,24,25 reported PBMC positivity ratios in stroke patients up to 87% by means of nested PCR without repetitive testing at all.…”

Section: Discussionmentioning

confidence: 99%

No Evidence of Involvement of Chlamydia pneumoniae in Severe Cerebrovascular Atherosclerosis by Means of Quantitative Real-Time Polymerase Chain Reaction

Apfalter

Barousch

Nehr

et al. 2004

Stroke

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Background and Purpose-All studies reporting high numbers of Chlamydia pneumoniae DNA positives in stroke patients published to date have used polymerase chain reaction (PCR) techniques highly prone to generate false-positive results. The aim of this study was to analyze the prevalence of C. pneumoniae DNA in plaques of the carotid artery as well as in peripheral blood by means of a new, closed, real-time PCR system. Methods-Carotid endarterectomy specimens and preoperative peripheral blood mononuclear cells (PBMC) of 75 individuals with severe cerebrovascular atherosclerosis were analyzed by means of a C. pneumoniae-specific quantitative ompA-based real-time PCR TaqMan system. Plaques were also cultured onto HEp-2 cells. Before the surgical intervention, C. pneumoniae-specific IgM, IgG, and IgA as well as C-reactive protein (CRP) levels were determined. Results-89% of all patients studied had C. pneumoniae-specific antibodies, but the pathogen was not detected in a single carotid atheroma by real-time PCR and cell culture. However, C. pneumoniae DNA was detected in 4 PBMC samples (5.3%) at very low levels (Ͻ1 inclusion/6 mL EDTA blood). No statistical significance was found between symptomatic/asymptomatic patients, C. pneumoniae PCR, results and CRP values after correction for multiplicity-oftest adjustment. Conclusions-By means of a closed, highly sensitive, and specific real-time PCR, C. pneumoniae was not detected in cerebrovascular atherosclerosis. PCR on PBMC was not predictive for endovascular chlamydia infection and most likely stem from previous C. pneumoniae respiratory tract infection in individual cases.

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“…89,97 C pneumoniae DNA was found in circulating leukocytes in patients with carotid stenosis but not in control subjects, and C pneumoniae DNA was more common than seropositivity. 98 It remains unclear whether C pneumoniae DNA correlates better with findings in plaques than serology. Seroepidemiological studies are limited by the high prevalence of antibodies in adults, by the failure to distinguish between subjects with prior infection and those with chronic infection, and by the discordance with findings in vessel walls.…”

Section: Continuous Inflammation In Matured Atherosclerotic Plaquesmentioning

confidence: 99%

Inflammation and Infections as Risk Factors for Ischemic Stroke

Lindsberg

Grau

2003

Stroke

462

312

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Background-Inflammatory processes have fundamental roles in stroke in both the etiology of ischemic cerebrovascular disease and the pathophysiology of cerebral ischemia. We summarize clinical data on infection and inflammation as risk or trigger factors for human stroke and investigate current evidence for the hypothesis of a functional interrelation between traditional risk factors, genetic predisposition, and infection/inflammation in stroke pathogenesis. Summary of Review-Several traditional vascular risk factors are associated with proinflammatory alterations, including leukocyte activation, and predispose cerebral vasculature to thrombogenesis on inflammatory stimulation. Furthermore, accumulation of inflammatory cells, mainly monocytes/macrophages, within the vascular wall starts early during atherogenesis. During later disease stages, their activation can lead to plaque rupture and thrombus formation, increasing stroke risk. Inflammatory markers (eg, leukocytes, fibrinogen, C-reactive protein) are independent predictors of ischemic stroke. Chronic infections (eg, infection with Chlamydia pneumoniae or Helicobacter pylori) were found to increase the risk of stroke; however, study results are at variance, residual confounding is not excluded, and causality is not established at present. In case-control studies, acute infection within the preceding week was a trigger factor for ischemic stroke. Acute and exacerbating chronic infection may act by activating coagulation and chronic infections and may contribute to atherogenesis. Genetic predisposition of the inflammatory host response may be an important codeterminant for atherogenesis and stroke risk. Conclusions-Inflammation contributes to stroke risk via various interrelated mechanisms. Infectious diseases, traditional risk factors, and genetic susceptibility may cooperate in stimulating inflammatory pathways. Final proof of a causal role of infectious/inflammatory mechanisms in stroke pathogenesis is still lacking and will require interventional studies.

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Chlamydia pneumoniae DNA in Peripheral Venous Blood Samples from Patients with Carotid Artery Stenosis

Cited by 14 publications

References 15 publications

Detection of CirculatingChlamydophila pneumoniaein Patients with Coronary Artery Disease and Healthy Control Subjects

Detection of CirculatingChlamydophila pneumoniaein Patients with Coronary Artery Disease and Healthy Control Subjects

No Evidence of Involvement of Chlamydia pneumoniae in Severe Cerebrovascular Atherosclerosis by Means of Quantitative Real-Time Polymerase Chain Reaction

Inflammation and Infections as Risk Factors for Ischemic Stroke

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