ArticleVirchows Archiv : an international journal of pathology2008
Amalgamation of Chlamydia pneumoniae inclusions with lipid droplets in foam cells in human atherosclerotic plaque.
Article in Virchows Archiv : an international journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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.
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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
6 citing papers in PubMed, 9 citations in OpenAlex.
- Lipid Droplets: A Significant but Understudied Contributor of Host⁻Bacterial Interactions.Cells · 2019Review
- Multiple Infectious Agents and the Origins of Atherosclerotic Coronary Artery Disease.Frontiers in cardiovascular medicine · 2016Review
- Laboratory diagnosis of persistent human chlamydial infection.Frontiers in cellular and infection microbiology · 2013Review
- Flotillin-1 (Reggie-2) contributes to Chlamydia pneumoniae growth and is associated with bacterial inclusion.Infection and immunity · 2012Article
- Analysis of Chlamydia pneumoniae infection in mononuclear cells by reverse transcription-PCR targeted to chlamydial gene transcripts.Medical microbiology and immunology · 2011Article
- Chlamydia pneumoniae-induced foam cell formation requires MyD88-dependent and -independent signaling and is reciprocally modulated by liver X receptor activation.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chlamydia pneumoniae (Chlamydophila pneumoniae) infect macrophages and accelerates foam cell formation in in vitro experiments, but whether this might occur in human atherosclerosis is unknown. In the present study, we examined 17 carotid artery segments, obtained by endarterectomy, in which the presence of C. pneumoniae was confirmed by both polymerase chain reaction and immunohistochemistry. Electron microscopy demonstrated the presence of structures with the appearance of elementary, reticulate and aberrant bodies of C. pneumoniae in the cytoplasm of macrophage foam cells. The volume of the cytoplasm that was free from vacuoles and lipid droplets in C. pneumoniae-infected foam cells was dramatically reduced, and a phenomenon of the amalgamation of C. pneumoniae inclusions with lipid droplets was detected. Double immunohistochemistry showed that C. pneumoniae-infected foam cells contained a large number of oxidized low-density lipoproteins. The observations provide support to the hypothesis that C. pneumoniae could affect foam cell formation in human atherosclerosis.
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Registered trials
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