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首页> 外文期刊>World Journal of Gastroenterology >Chlamydia pneumoniae replicates in Kupffer cells in mouse model of liver infection.
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Chlamydia pneumoniae replicates in Kupffer cells in mouse model of liver infection.

机译：在肝感染小鼠模型中，肺炎衣原体在库普弗细胞中复制。

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AIM: To develop an animal model of liver infection with Chlamydia pneumoniae (C. pneumoniae) in intraperitoneally infected mice for studying the presence of chlamydiae in Kupffer cells and hepatocytes. METHODS: A total of 80 BALB/c mice were inoculated intraperitoneally with C. pneumoniae and sacrificed at various time points after infection. Chlamydiae were looked for in liver homogenates as well as in Kupffer cells and hepatocytes separated by liver perfusion with collagenase. C. pneumoniae was detected by both isolation in LLC-MK2 cells and fluorescence in situ hybridization (FISH). The releasing of TNFA-alpha by C. pneumoniae in vitro stimulated Kupffer cells was studied by enzyme-linked immunosorbent assay. RESULTS: C. pneumoniae isolation from liver homogenates reached a plateau on d 7 after infection when 6 of 10 animals were positive, then decreased, and became negative by d 20. C. pneumoniae isolation from separated Kupffer cells reached a plateau on d 7 when 5 of 10 animals were positive, andbecame negative by d 20. The detection of C. pneumoniae in separated Kupffer cells by FISH, confirmed the results obtained by culture. Isolated hepatocytes were always negative. Stimulation of Kupffer cells by alive C. pneumoniae elicited high TNF-alpha levels. CONCLUSION: A productive infection by C. pneumoniae may take place in Kupffer cells and C. pneumoniae induces a local pro-inflammatory activity. C. pneumoniae is therefore, able to act as antigenic stimulus when localized in the liver. One could speculate that C. pneumoniae infection, involving cells of the innate immunity such as Kupffer cells, could also trigger pathological immune reactions involving the liver, as observed in human patients with primary biliary cirrhosis.
机译：目的：在腹膜内感染的小鼠体内建立肺炎衣原体（C. pneumoniae）肝感染的动物模型，以研究库普弗细胞和肝细胞中衣原体的存在。方法：共80只BALB / c小鼠腹膜内接种肺炎衣原体，并在感染后不同时间处死。在肝匀浆以及通过胶原酶肝灌注分离的库普弗细胞和肝细胞中寻找衣原体。通过在LLC-MK2细胞中分离和荧光原位杂交（FISH）均可检测到肺炎衣原体。通过酶联免疫吸附试验研究了肺炎衣原体体外刺激的枯否细胞释放TNFA-α。结果：从肝匀浆分离的肺炎衣原体在感染后第7天达到平台期，每10只动物中有6例呈阳性，然后下降，并在第20天变为阴性。 10只动物中有5只为阳性，而到d 20时为阴性。通过FISH检测分离的Kupffer细胞中的肺炎衣原体，证实了通过培养获得的结果。分离的肝细胞总是阴性的。活的肺炎衣原体刺激库普弗细胞引起高的TNF-α水平。结论：库普弗细胞中可能发生肺炎衣原体的生产性感染，并且肺炎衣原体诱导了局部促炎活性。因此，肺炎衣原体在肝脏中定位时能够充当抗原刺激。人们可以推测，涉及人类先天性胆汁性肝硬化的患者中发现，涉及固有免疫力的细胞（如库普弗细胞）的肺炎衣原体感染也可能引发涉及肝脏的病理性免疫反应。

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