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铜绿假单胞菌产生的群体感应信号分子导致尿路感染小鼠模型中的炎症和逃避宿主因子。

Quorum sensing signal molecules produced by Pseudomonas aeruginosa cause inflammation and escape host factors in murine model of urinary tract infection.

机构信息

Department of Microbiology, BMS Block, Panjab University, Chandigarh, India, 160014.

出版信息

Inflammation. 2013 Oct;36(5):1153-9. doi: 10.1007/s10753-013-9650-y.

DOI:10.1007/s10753-013-9650-y
PMID:23636638
Abstract

Quorum sensing (QS) is well established for its role in pathogenesis of various infections of Pseudomonas aeruginosa. However, its role in local tissue damage during urinary tract infection (UTI) is not yet fully established. To have insight in this, the present study was planned. UTI was established in mice using standard strain PAO1 and its isogenic QS mutant JP2. One group was challenged only with QS signals. Damage was assessed in terms of histopathology and pathology markers, malondialdehyde (MDA) and reactive nitrogen intermediates (RNI). Effect on pathogen motility, uroepithelial adhesion, and host serum sensitivity was also ascertained. PAO1-infected mice showed severe inflammation and tissue destruction, while mice infected with JP2 showed no significant destruction. JP2 was also unable to mount any tissue pathology markers, MDA and RNI, whereas PAO1 showed significantly higher levels of these two. Presence of only QS signals also showed considerable renal pathology. Strain JP2 also showed less motility, reduced uroepithelial cell adhesion, and increased serum sensitivity. Result highlights that QS signals induce local tissue pathology along with interference of host protective mechanisms during UTI.

摘要

群体感应(QS)在铜绿假单胞菌的各种感染的发病机制中起着重要作用。然而,其在尿路感染(UTI)期间局部组织损伤中的作用尚未完全确定。为了深入了解这一点,进行了本研究。使用标准菌株 PAO1 和其同源 QS 突变体 JP2 在小鼠中建立 UTI。一组仅受到 QS 信号的挑战。通过组织病理学和病理学标志物、丙二醛(MDA)和活性氮中间产物(RNI)来评估损伤。还确定了对病原体运动性、尿路上皮黏附性和宿主血清敏感性的影响。PAO1 感染的小鼠表现出严重的炎症和组织破坏,而 JP2 感染的小鼠则没有明显的破坏。JP2 也无法产生任何组织病理学标志物、MDA 和 RNI,而 PAO1 则显示出这两种标志物的水平显著升高。仅存在 QS 信号也会引起相当大的肾脏病理学。JP2 菌株还表现出较低的运动性、减少的尿路上皮细胞黏附性和增加的血清敏感性。结果强调了 QS 信号在 UTI 期间会引起局部组织病理学以及干扰宿主保护机制。

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PLoS One. 2011 Jan 31;6(1):e16246. doi: 10.1371/journal.pone.0016246.
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