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Correlation between rises in Chlamydia pneumoniae-specific antibodies, platelet activation and lipid peroxidation after percutaneous coronary intervention.
Linköping University, Department of Medicine and Health Sciences, Pharmacology . Linköping University, Faculty of Health Sciences.
Linköping University, Department of Medicine and Health Sciences, Pharmacology . Linköping University, Faculty of Health Sciences.
Linköping University, Department of Medicine and Health Sciences, Division of Preventive and Social Medicine and Public Health Science. Linköping University, Faculty of Health Sciences.
(Department of Cardiology, Linköping University Hospital, Linköping, Sweden)
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2008 (English)In: European Journal of Clinical Microbiology and Infectious Diseases, ISSN 0934-9723, E-ISSN 1435-4373, Vol. 27, no 7, 503-511 p.Article in journal (Refereed) Published
Abstract [en]

We recently showed that Chlamydia pneumoniae activates platelets in vitro, with an associated oxidation of low-density lipoproteins. The aim of this study was to investigate whether C. pneumoniae is released during percutaneous coronary intervention (PCI) and, thereby, causes platelet activation and lipid peroxidation. Seventy-three patients undergoing coronary angiography and following PCI or coronary artery bypass graft (CABG) and 57 controls were included in the study. C. pneumoniae antibodies, serotonin and lipid peroxidation were measured before and 24 h, 1 month and 6 months after angiography. The results show that serum C. pneumoniae IgA concentrations were significantly higher in patients than in the controls. Furthermore, in 38% of the C. pneumoniae IgG positive patients, the C. pneumoniae IgG concentration increased 1 month after PCI. The levels of C. pneumoniae IgG antibodies 1 month after PCI correlated with plasma-lipid peroxidation (r = 0.91, P < 0.0001) and platelet-derived serotonin (r = 0.62, P = 0.02). There was no elevation in the total serum IgG 1 month after PCI. In conclusion, the present results suggest that PCI treatment of coronary stenosis releases C. pneumoniae from the atherosclerotic lesions, which leads to platelet activation and lipid peroxidation.

Place, publisher, year, edition, pages
2008. Vol. 27, no 7, 503-511 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-14388DOI: 10.1007/s10096-008-0465-yOAI: oai:DiVA.org:liu-14388DiVA: diva2:23383
Available from: 2007-04-20 Created: 2007-04-20 Last updated: 2017-12-13Bibliographically approved
In thesis
1. The Role of Chlamydia pneumoniae-induced Platelet Activation in Cardiovascular Disease: In vitro and In vivo studies
Open this publication in new window or tab >>The Role of Chlamydia pneumoniae-induced Platelet Activation in Cardiovascular Disease: In vitro and In vivo studies
2007 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The common risk factors for atherosclerosis, such as obesity, high cholesterol levels, sedentary lifestyle, diabetes and high alcohol intake, only explain approximately 50% of cardiovascular disease events. It is thereby important to identify new mechanisms that can stimulate the process of atherosclerosis. During the past decades, a wide range of investigations have demonstrated connections between infections by the respiratory bacterium Chlamydia pneumoniae and atherosclerosis. Earlier studies have focused on the interaction between C. pneumoniae and monocytes/macrophages, T-lymphocytes, smooth muscle cells and endothelial cells, which are present in the atherosclerotic plaque. However, another important player in atherosclerosis and which is also present in the plaques is the platelet. Activation of platelets can stimulate both initiation and progression of atherosclerosis and thrombosis, which is the ultimate endpoint of the disease. The aim of the present thesis was to investigate the capacity of C. pneumoniae to activate platelets and its role in atherosclerosis.

The results show that C. pneumoniae at low concentrations binds to platelets and stimulates platelet aggregation, secretion, reactive oxygen species (ROS) production and oxidation of low-density lipoproteins (LDL), and that these effects are mediated by lipopolysaccharide (LPS). Activation of protein kinase C, nitric oxide synthase and 12-lipoxygenase (12-LOX) was required for platelet ROS production, whereas platelet aggregation was dependent on activation of GpIIb/IIIa. Pharmacological studies showed that the C. pneumoniae-induced platelet activation is prevented by inhibitors against 12-LOX, platelet activating factor (PAF) and the purinergic P2Y1 and P2Y12 receptors, but not against cyclooxygenase (COX). These findings were completely opposite to the effects of these inhibitors on collagen-stimulated platelets. We also present data from a clinical study indicating that percutaneous coronary intervention (PCI or balloon dilatation) leads to release of C. pneumoniae into the circulation, which causes platelet activation and LDL oxidation.

In conclusion, these data support a role for C. pneumoniae-induced platelet activation in the process of atherosclerosis. Stimulation of platelets by C. pneumoniae leads to release of growth factors and cytokines, oxidation of LDL and platelet aggregation, which are processes that can stimulate both atherosclerosis and thrombosis. Development of novel drugs that prevent C. pneumoniae-platelet interaction by inhibiting 12-LOX and/or PAF, may be important in the future treatment of cardiovascular disease.

Place, publisher, year, edition, pages
Institutionen för medicin och vård, 2007
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 995
Keyword
Chlamydia pneumoniae, Platelet, atherosclerosis, Infection, LDL-oxidation, Percutaneous coronary intervention, Cardiovascular disease, Serotonin, Reactive oxygen species production
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:liu:diva-8643 (URN)978-91-85715-32-9 (ISBN)
Public defence
2007-05-11, Berzeliussalen, hus 420, Campus US, Linköpings universitet, Linköping, 09:00 (English)
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Available from: 2007-04-20 Created: 2007-04-20 Last updated: 2009-08-22

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Kälvegren, HannaFridfeldt (Berggren), JonnaGarvin, PeterLeanderson, PerKristenson, MargarethaKihlström, ErikBengtsson, TorbjörnRichter, Arina

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Kälvegren, HannaFridfeldt (Berggren), JonnaGarvin, PeterLeanderson, PerKristenson, MargarethaKihlström, ErikBengtsson, TorbjörnRichter, Arina
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Pharmacology Faculty of Health SciencesDivision of Preventive and Social Medicine and Public Health ScienceOccupational and Environmental Medicine Clinical Microbiology Cardiology
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