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控制小鼠肺炎克雷伯菌黏膜定植的宿主和微生物群因素。

Host and microbiota factors that control Klebsiella pneumoniae mucosal colonization in mice.

作者信息

Lau Helen Y, Huffnagle Gary B, Moore Thomas A

机构信息

Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109, USA.

出版信息

Microbes Infect. 2008 Oct;10(12-13):1283-90. doi: 10.1016/j.micinf.2008.07.040. Epub 2008 Aug 13.

DOI:10.1016/j.micinf.2008.07.040
PMID:18762269
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2633640/
Abstract

Klebsiella pneumoniae is both an opportunistic pathogen and a commensal organism. We have previously reported that K. pneumoniae strain IA565 (KpIA565) is non-pathogenic in a murine model of acute pneumonia. In this study, KpIA565 was inoculated into wild-type mice and found to stably colonize and persist in the nasal cavity and gastrointestinal tract of mice for up to 3weeks post-inoculation. Intranasal inoculation of wild-type or germ-free mice with KpIA565 resulted in similar bacterial levels in the nasal cavity, suggesting KpIA565 nasal colonization is independent of normal nasal microbiota. In contrast, KpIA565 gastrointestinal tract colonization was significantly higher in germ-free mice than in wild-type mice, indicating that members of the endogenous microbiota regulate KpIA565 colonization. In the presence of non-specific dextran sodium sulfate-induced inflammation, KpIA565 gastrointestinal tract colonization was significantly higher when compared to non-DSS treated mice. Interestingly, KpIA565 colonization was unaffected by Citrobacter rodentium-induced gastrointestinal tract inflammation. However, gastrointestinal tract colonization with K. pneumoniae strain IA565 had no impact on the inflammatory histopathology in either colitis model. This study is the first to identify and describe mechanisms influencing the growth and behavior of a murine commensal strain of K. pneumoniae.

摘要

肺炎克雷伯菌既是一种机会致病菌,也是一种共生生物。我们之前报道过,肺炎克雷伯菌IA565菌株(KpIA565)在急性肺炎小鼠模型中无致病性。在本研究中,将KpIA565接种到野生型小鼠体内,发现其在接种后长达3周的时间里能在小鼠的鼻腔和胃肠道中稳定定殖并持续存在。用KpIA565对野生型或无菌小鼠进行鼻内接种,鼻腔内细菌水平相似,这表明KpIA565在鼻腔的定殖独立于正常的鼻腔微生物群。相比之下,无菌小鼠中KpIA565在胃肠道的定殖明显高于野生型小鼠,这表明内源性微生物群成员调节KpIA565的定殖。在非特异性葡聚糖硫酸钠诱导的炎症存在的情况下,与未用葡聚糖硫酸钠处理的小鼠相比,KpIA565在胃肠道的定殖明显更高。有趣的是,KpIA565的定殖不受鼠柠檬酸杆菌诱导的胃肠道炎症的影响。然而,肺炎克雷伯菌IA565菌株在胃肠道的定殖对两种结肠炎模型中的炎症组织病理学均无影响。本研究首次鉴定并描述了影响肺炎克雷伯菌小鼠共生菌株生长和行为的机制。

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Host-mediated inflammation disrupts the intestinal microbiota and promotes the overgrowth of Enterobacteriaceae.宿主介导的炎症会破坏肠道微生物群并促进肠杆菌科细菌过度生长。
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