4.6 Article

The sensor kinase BfmS controls production of outer membrane vesicles in Acinetobacter baumannii

期刊

BMC MICROBIOLOGY
卷 19, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12866-019-1679-0

关键词

Acinetobacter baumannii; BfmS; Cytotoxicity; OmpA; Outer membrane vesicle

资金

  1. National Research Foundation of Korea (NRF) - Korea government [NRF-2017R1A2A2A05001014]
  2. Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI) - Ministry of Health & Welfare, Republic of Korea [HI17C1657]

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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, Delta bfmS mutant, and bfmS-complemented strains. Results The Delta bfmS 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 Delta bfmS 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 Delta bfmS mutant produced 2.35 times more OMV particles and 4.46 times more OMV proteins than the wild-type stain. The Delta bfmS 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.

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