Source:http://linkedlifedata.com/resource/pubmed/id/19822082
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
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| pubmed:dateCreated |
2009-10-13
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| pubmed:abstractText |
Chlamydia pneumoniae persistent infection has been implicated in the pathogenesis of several chronic inflammatory diseases including atherosclerosis, and we hypothesized that modulation of the apoptosis of macrophages and/or T cells by C. pneumoniae infection may contribute to the development of such diseases. We therefore evaluated apoptosis, cytokine response, and redox status in human primary T cells and macrophages infected with C. pneumoniae. In addition, co-cultures of T cells and macrophages infected with C. pneumoniae were also carried out. Apoptosis, and levels of glutathione (GSH), glutathione disulfide (GSSG), and tumour necrosis factor (TNF)-alpha were measured by flow cytometry, high performance liquid chromatography and enzyme-linked immunosorbent assay. C. pneumoniae induced apoptosis in T cells as well as in co-cultures of T cells and infected macrophages by marked decrease in GSH/GSSG ratio and increased production of TNF-alpha, respectively. The results demonstrate that interaction of C. pneumoniae with T cells and/or macrophages characterized by interference with redox status, and secretion of tumour necrosis factor-alpha culminates in the induction of T cell apoptosis and survival of infected macrophages. In conclusion, the inappropriate T cell response against C. pneumoniae and survival of infected macrophages could explain the persistence of this intracellular obligate pathogen in the host-organism; it may contribute to the development of chronic inflammatory diseases, although further studies are needed to clarify such a complex mechanism.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
0394-6320
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
22
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
659-68
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| pubmed:meshHeading |
pubmed-meshheading:19822082-Apoptosis,
pubmed-meshheading:19822082-Cell Line,
pubmed-meshheading:19822082-Cell Survival,
pubmed-meshheading:19822082-Chlamydophila pneumoniae,
pubmed-meshheading:19822082-Chromatography, High Pressure Liquid,
pubmed-meshheading:19822082-Coculture Techniques,
pubmed-meshheading:19822082-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:19822082-Flow Cytometry,
pubmed-meshheading:19822082-Glutathione,
pubmed-meshheading:19822082-Glutathione Disulfide,
pubmed-meshheading:19822082-Humans,
pubmed-meshheading:19822082-Macrophages,
pubmed-meshheading:19822082-Oxidation-Reduction,
pubmed-meshheading:19822082-Signal Transduction,
pubmed-meshheading:19822082-T-Lymphocytes,
pubmed-meshheading:19822082-Tumor Necrosis Factor-alpha,
pubmed-meshheading:19822082-Up-Regulation
|
| pubmed:articleTitle |
Chlamydia pneumoniae induces T cell apoptosis through glutathione redox imbalance and secretion of TNF-alpha.
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| pubmed:affiliation |
Department of Public Health Sciences, Sapienza University, Rome, Italy.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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