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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Progression of primary pneumonic plague: a mouse model of infection, pathology, and bacterial transcriptional activity.
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Progression of primary pneumonic plague: a mouse model of infection, pathology, and bacterial transcriptional activity.

机译：原发性肺鼠疫的进展：感染，病理和细菌转录活性的小鼠模型。

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摘要

Although pneumonic plague is the deadliest manifestation of disease caused by the bacterium Yersinia pestis, there is surprisingly little information on the cellular and molecular mechanisms responsible for Y. pestis-triggered pathology in the lung. Therefore, to understand the progression of this unique disease, we characterized an intranasal mouse model of primary pneumonic plague. Mice succumbed to a purulent multifocal severe exudative bronchopneumonia that closely resembles the disease observed in humans. Analyses revealed a strikingly biphasic syndrome, in which the infection begins with an antiinflammatory state in the first 24-36 h that rapidly progresses to a highly proinflammatory state by 48 h and death by 3 days. To assess the adaptation of Y. pestis to a mammalian environment, we used DNA microarray technology to analyze the transcriptional responses of the bacteria during interaction with the mouse lung. Included among the genes up-regulated in vivo are those comprising the yop-ysc type III secretion system and genes contained within the chromosomal pigmentation locus, validating the use of this technology to identify loci essential to the virulence of Y. pestis.
机译：尽管肺鼠疫是由鼠疫耶尔森氏菌引起的最致命的疾病表现，但令人惊讶的是，关于造成鼠疫耶尔森氏菌触发的肺部病理的细胞和分子机制的信息却很少。因此，为了了解这种独特疾病的进展，我们表征了原发性肺鼠疫的鼻内小鼠模型。小鼠死于化脓性多灶性严重渗出性支气管肺炎，与人类观察到的疾病极为相似。分析揭示了一种惊人的双相综合征，其中感染在最初的24-36小时内以抗炎状态开始，到48小时迅速发展为高度促炎状态，并在3天后死亡。为了评估鼠疫耶尔森氏菌对哺乳动物环境的适应性，我们使用了DNA微阵列技术来分析细菌与小鼠肺部相互作用期间的转录反应。在体内上调的基因中包括那些包含yop-ysc III型分泌系统的基因和包含在染色体色素沉着基因座中的基因，这证实了该技术的使用以鉴定对鼠疫耶尔森氏菌的毒力至关重要的基因座。

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