ArticleBMC infectious diseases2006
Tissue MicroArray (TMA) analysis of normal and persistent Chlamydophila pneumoniae infection.
Article in BMC infectious diseases, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 1 citations in OpenAlex.
- Article
- Detection of Chlamydophila psittaci from pigeons by polymerase chain reaction in Ahvaz.Iranian journal of microbiology · 2015Article
- Evolution to a chronic disease niche correlates with increased sensitivity to tryptophan availability for the obligate intracellular bacterium Chlamydia pneumoniae.Journal of bacteriology · 2014Review
- Persistent C. pneumoniae infection in atherosclerotic lesions: rethinking the clinical trials.Frontiers in cellular and infection microbiology · 2014Review
- Chlamydia in canine or feline coronary arteriosclerotic lesions.BMC research notes · 2011Article
- Parachlamydia spp. and related Chlamydia-like organisms and bovine abortion.Emerging infectious diseases · 2007Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundChlamydophila pneumoniae infection has been implicated as a potential risk factor for atherosclerosis, however the mechanism leading to persistent infection and its role in the disease process remains to be elucidated.
methodsWe validated the use of tissue microarray (TMA) technology, in combination with immunohistochemistry (IHC), to test antibodies (GroEL, GroES, GspD, Ndk and Pyk) raised against differentially expressed proteins under an interferon-gamma (IFN-gamma) induced model of chlamydial persistence.
resultsIn the cell pellet array, we were able to identify differences in protein expression patterns between untreated and IFN-gamma treated samples. Typical, large chlamydial inclusions could be observed in the untreated samples with all antibodies, whereas the number of inclusions were decreased and were smaller and atypical in shape in the IFN-gamma treated samples. The staining results obtained with the TMA method were generally similar to the changes observed between normal and IFN-gamma persistence using proteomic analysis. Subsequently, it was shown in a second TMA including archival atheromatous heart tissues from 12 patients undergoing heart transplantation, that GroEL, GroES, GspD and Pyk were expressed in atheromatous heart tissue specimens as well, and were detectable morphologically within lesions by IHC.
conclusionTMA technology proved useful in documenting functional proteomics data with the morphologic distribution of GroEL, GroES, GspD, Ndk and Pyk within formalin-fixed, paraffin-embedded cell pellets and tissues from patients with severe coronary atherosclerosis. The antibodies GroEL and GroES, which were upregulated under persistence in proteomic analysis, displayed positive reaction in atheromatous heart tissue from 10 out of 12 patients. These may be useful markers for the detection of persistent infection in vitro and in vivo.
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