Quantitative analysis of propionibacterial DNA in bronchoalveolar lavage cells from patients with sarcoidosis.

Quantitative analysis of propionibacterial DNA in bronchoalveolar lavage cells from patients with sarcoidosis.
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发表时间:
2008-06
期刊:
Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG
影响因子:
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通讯作者:
H. Ichikawa;M. Kataoka;J. Hiramatsu;M. Ohmori;Y. Tanimoto;A. Kanehiro;Yasunari Nakata;M. Tanimoto
H. Ichikawa;M. Kataoka;J. Hiramatsu;M. Ohmori;Y. Tanimoto;A. Kanehiro;Yasunari Nakata;M. Tanimoto
中科院分区:
其他
文献类型:
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作者:
H. Ichikawa;M. Kataoka;J. Hiramatsu;M. Ohmori;Y. Tanimoto;A. Kanehiro;Yasunari Nakata;M. Tanimoto

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背景和目的结节病的病因至今仍不清楚。丙酸杆菌亚种被认为是最可能的抗原来源之一。在这里,我们试图测量结节病和其他肺部疾病患者支气管肺泡灌洗(BAL)细胞样本中丙酸杆菌DNA的量。方法我们检测了42例结节病患者和30例对照的BAL细胞。采用定量聚合酶链反应(PCR)检测痤疮丙酸杆菌(P. acnes)和颗粒丙酸杆菌(P. granulosum)的16 S rRNA,我们测量了从结节病或其他肺部疾病患者的BAL细胞中提取的500 ng总DNA中丙酸杆菌DNA的量。分析临床表现与定量PCR结果的相关性。结果结节病患者痤疮丙酸杆菌DNA平均含量为59.9个基因组/500 ng总DNA,显著高于对照组(20.7个基因组,p<0.0001)。结节病患者的颗粒变形杆菌DNA平均水平为1.2个基因组,与对照组相似(1.0 +/-1.6个基因组,p=0.52)。结节病患者BAL细胞中痤疮丙酸杆菌的基因组数量与血清血管紧张素转换酶(ACE)水平和BAL液中巨噬细胞的百分比相关。结论结节病患者BAL细胞中痤疮丙酸杆菌DNA含量明显高于其他肺部疾病患者。痤疮丙酸杆菌可能参与结节病的发病机制。
BACKGROUND AND AIM OF THE WORK The causes of sarcoidosis are still unknown. Propionibacterial subspieces are thought to be one of the most likely sources of antigens. Here we attempted to measure the amount of propionibacterial DNA in bronchoalveolar lavage (BAL) cell samples from patients with sarcoidosis and other pulmonary diseases. METHODS We examined BAL cells from 42 patients with sarcoidosis and 30 controls. Using quantitative polymerase chain reaction (PCR) for 16S rRNA of Propionibacterium acnes (P. acnes) and Propionibacterium granulosum (P. granulosum), we measured the amount of propionibacterial DNA in 500 ng of total DNA extracted from BAL cells from patients with sarcoidosis or other lung diseases. The correlation between clinical findings and the results of quantitative PCR were analyzed. RESULTS The mean level of P. acnes DNA from patients with sarcoidosis was 59.9 genomes per 500 ng of total DNA, which was significantly higher than that in controls (20.7 genomes, p<0.000l). The mean level of P. granulosum DNA from patients with sarcoidosis was 1.2 genomes, which was similar to that in controls (1.0 +/-1.6 genomes, p=0.52). The number of genomes of P. acnes in BAL cells was correlated with the serum angiotensin-converting enzyme (ACE) level and the percentage of macrophages in BAL fluid from patients with sarcoidosis. CONCLUSIONS The amount of P. acnes DNA in BAL cells from patients with sarcoidosis was significantly higher than that in BAL cells from patients with other pulmonary diseases. P. acnes may be involved in the pathogenesis of sarcoidosis.