BACKGROUND Acinetobacter baumannii is an important opportunistic pathogen responsible for various nosocomial infections. The BfmRS two-component system plays a role in pathogenesis and antimicrobial resistance of A. baumannii via regulation of bacterial envelope structures. This study investigated the role of the sensor kinase, BfmS, in localization of outer membrane protein A (OmpA) in the outer membrane and production of outer membrane vesicles (OMVs) using wild-type A. baumannii ATCC 17978, ΔbfmS mutant, and bfmS-complemented strains. RESULTS The ΔbfmS mutant showed hypermucoid phenotype in the culture plates, growth retardation under static culture conditions, and reduced susceptibility to aztreonam and colistin compared to the wild-type strain. The ΔbfmS mutant produced less OmpA in the outer membrane but released more OmpA via OMVs than the wild-type strain, even though expression of ompA and its protein production were not different between the two strains. The ΔbfmS mutant produced 2.35 times more OMV particles and 4.46 times more OMV proteins than the wild-type stain. The ΔbfmS mutant OMVs were more cytotoxic towards A549 cells than wild-type strain OMVs. CONCLUSIONS The present study demonstrates that BfmS controls production of OMVs in A. baumannii. Moreover, BfmS negatively regulates antimicrobial resistance of A. baumannii and OMV-mediated host cell cytotoxicity. Our results indicate that BfmS negatively controls the pathogenic traits of A. baumannii via cell envelope structures and OMV production.

中文翻译：

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传感器激酶BfmS控制鲍曼不动杆菌中外膜囊泡的产生。

背景技术鲍曼不动杆菌是引起各种医院感染的重要机会病原体。BfmRS两组分系统通过调节细菌包膜结构，在鲍氏不动杆菌的发病机理和抗药性中发挥作用。这项研究调查了传感器激酶BfmS在使用野生型A.baumannii ATCC 17978，ΔbfmS突变体和bfmS在外膜中定位外膜蛋白A（OmpA）和生产外膜囊泡（OMV）中的作用-互补菌株。结果与野生型菌株相比，ΔbfmS突变体在培养板中表现出超粘液表型，在静态培养条件下生长迟缓，对氨曲南和粘菌素的敏感性降低。ΔbfmS突变体在外膜中产生的OmpA较少，但通过OMV释放的OmpA却比野生型菌株多，即使这两个菌株之间ompA的表达及其蛋白产量没有差异。与野生型染色剂相比，ΔbfmS突变体产生的OMV颗粒多2.35倍，OMV蛋白多4.46倍。ΔbfmS突变体OMV比野生型菌株OMV对A549细胞具有更高的细胞毒性。结论本研究表明BfmS控制鲍曼不动杆菌中OMV的产生。此外，BfmS负调节鲍曼不动杆菌的抗药性和OMV介导的宿主细胞的细胞毒性。我们的结果表明BfmS通过细胞包膜结构和OMV产生负控制鲍曼不动杆菌的致病性状。即使两种菌株之间的ompA表达及其蛋白产量没有差异。与野生型染色剂相比，ΔbfmS突变体产生的OMV颗粒多2.35倍，OMV蛋白多4.46倍。ΔbfmS突变体OMV比野生型菌株OMV对A549细胞具有更高的细胞毒性。结论本研究证明BfmS控制鲍曼不动杆菌中OMV的产生。此外，BfmS负调节鲍曼不动杆菌的抗药性和OMV介导的宿主细胞的细胞毒性。我们的结果表明BfmS通过细胞包膜结构和OMV产生负控制鲍曼不动杆菌的致病性状。即使ompA的表达及其蛋白产量在两个菌株之间没有差异。与野生型染色剂相比，ΔbfmS突变体产生的OMV颗粒多2.35倍，OMV蛋白多4.46倍。ΔbfmS突变体OMV比野生型菌株OMV对A549细胞具有更高的细胞毒性。结论本研究证明BfmS控制鲍曼不动杆菌中OMV的产生。此外，BfmS负调节鲍曼不动杆菌的抗药性和OMV介导的宿主细胞的细胞毒性。我们的结果表明BfmS通过细胞包膜结构和OMV产生负控制鲍曼不动杆菌的致病性状。ΔbfmS突变体OMV比野生型菌株OMV对A549细胞具有更高的细胞毒性。结论本研究证明BfmS控制鲍曼不动杆菌中OMV的产生。此外，BfmS负调节鲍曼不动杆菌的抗药性和OMV介导的宿主细胞的细胞毒性。我们的结果表明BfmS通过细胞包膜结构和OMV产生负控制鲍曼不动杆菌的致病性状。ΔbfmS突变体OMV比野生型菌株OMV对A549细胞具有更高的细胞毒性。结论本研究证明BfmS控制鲍曼不动杆菌中OMV的产生。此外，BfmS负调节鲍曼不动杆菌的抗药性和OMV介导的宿主细胞的细胞毒性。我们的结果表明BfmS通过细胞包膜结构和OMV产生负控制鲍曼不动杆菌的致病性状。