| Autor: |
Renko, Jaana, Kalela, A., Karhunen, P. J., Helin, H., Sillanaukee, P., Nikkari, S., Nikkari, S.T. |
| Jazyk: |
angličtina |
| Rok vydání: |
2003 |
| Předmět: |
|
| Zdroj: |
Renko, J, Kalela, A, Karhunen, P J, Helin, H, Sillanaukee, P, Nikkari, S & Nikkari, S T 2003, ' Do temporal arteritis lesions contain bacterial DNA? ', European Journal of Clinical Investigation, vol. 33, no. 8, pp. 657-61 . https://doi.org/10.1046/j.1365-2362.2003.01199.x |
| DOI: |
10.1046/j.1365-2362.2003.01199.x |
| Popis: |
BACKGROUND: Temporal arteritis is a primary vascular inflammatory disease. The aetiology of temporal arteritis is unknown, but the influence of environmental factors such as infections has been suggested.MATERIALS AND METHODS: We used broad-range PCR, targeting conserved regions of the gene encoding for ribosomal RNA, to detect bacterial DNA in 27 temporal artery biopsies. Five uninvolved temporal arteries were also included. A lung sample of confirmed bacterial pneumonia served as a positive control. Inflammation was examined by histochemistry and light microscopy.RESULTS: The sensitivity of the broad-range PCR assay was 5.0 fg of DNA. Bacterial DNA sequences were neither detected in 27 temporal arteritis specimens nor in the normal temporal artery samples. However, bacterial DNA was successfully amplified from the lung sample of a subject with pneumonia. In addition, human DNA was amplified by primers for human beta-actin from all clinical specimens, suggesting lack of significant inhibitors of the molecular amplification reaction. Histochemistry showed signs of strong inflammation in the arteritis samples.CONCLUSIONS: The lack of detectable amounts of bacterial DNA suggests that viable bacteria do not have a role in chronic stages of temporal arteritis. However, these findings do not rule out the possibility of bacterial degradation products as stimulants of chronic inflammation, or of viable microbes as triggering factors of acute temporal arteritis. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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