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磷脂酶 D 的失活可降低鲍曼不动杆菌的发病机制。

Inactivation of phospholipase D diminishes Acinetobacter baumannii pathogenesis.

机构信息

Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198-5900, USA.

出版信息

Infect Immun. 2010 May;78(5):1952-62. doi: 10.1128/IAI.00889-09. Epub 2010 Mar 1.

Abstract

Acinetobacter baumannii is an emerging bacterial pathogen of considerable health care concern. Nonetheless, relatively little is known about the organism's virulence factors or their regulatory networks. Septicemia and ventilator-associated pneumonia are two of the more severe forms of A. baumannii disease. To identify virulence factors that may contribute to these disease processes, genetically diverse A. baumannii clinical isolates were evaluated for the ability to proliferate in human serum. A transposon mutant library was created in a strain background that propagated well in serum and screened for members with decreased serum growth. The results revealed that disruption of A. baumannii phospholipase D (PLD) caused a reduction in the organism's ability to thrive in serum, a deficiency in epithelial cell invasion, and diminished pathogenesis in a murine model of pneumonia. Collectively, these results suggest that PLD is an A. baumannii virulence factor.

摘要

鲍曼不动杆菌是一种具有相当健康护理关注的新兴细菌病原体。尽管如此,人们对该生物体的毒力因子或其调控网络知之甚少。败血症和呼吸机相关性肺炎是鲍曼不动杆菌病的两种更严重形式。为了确定可能导致这些疾病过程的毒力因子,评估了具有遗传多样性的鲍曼不动杆菌临床分离株在人血清中增殖的能力。在一种在血清中繁殖良好的菌株背景下创建了转座子突变体文库,并筛选了血清生长减少的成员。结果表明,破坏鲍曼不动杆菌磷脂酶 D(PLD)会降低该生物体在血清中茁壮成长的能力、上皮细胞侵袭能力的缺陷以及肺炎小鼠模型中的发病机制减弱。总的来说,这些结果表明 PLD 是鲍曼不动杆菌的一种毒力因子。

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