ArticlePloS one2010
Association of carotid plaque Lp-PLA(2) with macrophages and Chlamydia pneumoniae infection among patients at risk for stroke.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Chlamydia pneumoniae-Mediated Inflammation in Atherosclerosis: A Meta-Analysis.Mediators of inflammation · 2015Pooled it
- Lipoprotein-associated Phospholipase A2 Is Associated with Risk of Mild Cognitive Impairment in Chinese Patients with Type 2 Diabetes.Scientific reports · 2017Article
- Research Progress on the Risk Factors and Outcomes of Human Carotid Atherosclerotic Plaques.Chinese medical journal · 2017Review
- Circulating Lp-PLA₂ activity correlates with oxidative stress and cytokines in overweight/obese postmenopausal women not using hormone replacement therapy.Age (Dordrecht, Netherlands) · 2015Article
- Chlamydia pneumoniae Clinical Isolate from Gingival Crevicular Fluid: A Potential Atherogenic Strain.Frontiers in cellular and infection microbiology · 2015Article
- Chlamydia pneumoniae and oxidative stress in cardiovascular disease: state of the art and prevention strategies.International journal of molecular sciences · 2014Review
- Mannan-binding lectin in cardiovascular disease.BioMed research international · 2014Review
- Chlamydia pneumoniae infection in atherosclerotic lesion development through oxidative stress: a brief overview.International journal of molecular sciences · 2013Review
- Chlamydophila pneumoniae infection and cardiovascular disease.North American journal of medical sciences · 2013Article
- Osteocalcin positive CD133+/CD34-/KDR+ progenitor cells as an independent marker for unstable atherosclerosis.European heart journal · 2012Article
- Translational studies of lipoprotein-associated phospholipase A₂ in inflammation and atherosclerosis.Journal of the American College of Cardiology · 2012Article
- Lipoprotein-associated phospholipase A2 activity predicts cardiovascular events in high risk coronary artery disease patients.PloS one · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWe previously showed that the burden of Chlamydia pneumoniae in carotid plaques was significantly associated with plaque interleukin (IL)-6, and serum IL-6 and C-reactive protein (CRP), suggesting that infected plaques contribute to systemic inflammatory markers in patients with stroke risk. Since lipoprotein-associated phospholipase A2 (Lp-PLA(2)) mediates inflammation in atherosclerosis, we hypothesized that serum Lp-PLA(2) mass and activity levels and plaque Lp-PLA(2) may be influenced by plaque C. pneumoniae infection. METHODOLOGY/PRINCIPAL
findingsForty-two patients underwent elective carotid endarterectomy. Tissue obtained at surgery was stained by immunohistochemistry for Lp-PLA(2) grade, macrophages, IL-6, C. pneumoniae and CD4+ and CD8+ cells. Serum Lp-PLA(2) activity and mass were measured using the colorimetric activity method (CAM) and ELISA, respectively. Serum homocysteine levels were measured by HPLC. Eleven (26.2%) patients were symptomatic with transient ischemic attacks. There was no correlation between patient risk factors (smoking, coronary artery disease, elevated cholesterol, diabetes, obesity, hypertension and family history of genetic disorders) for atherosclerosis and serum levels or plaque grade for Lp-PLA(2). Plaque Lp-PLA(2) correlated with serum homocysteine levels (p = 0.013), plaque macrophages (p<0.01), and plaque C. pneumoniae (p<0.001), which predominantly infected macrophages, co-localizing with Lp-PLA(2).
conclusionsThe significant association of plaque Lp-PLA(2) with plaque macrophages and C. pneumoniae suggests an interactive role in accelerating inflammation in atherosclerosis. A possible mechanism for C. pneumoniae in the atherogenic process may involve infection of macrophages that induce Lp-PLA(2) production leading to upregulation of inflammatory mediators in plaque tissue. Additional in vitro and in vivo research will be needed to advance our understanding of specific C. pneumoniae and Lp-PLA(2) interactions in atherosclerosis.
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