Abstract
BackgroundAcinetobacter 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.ResultsThe 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.ConclusionsThe 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.
Highlights
Acinetobacter baumannii is an important opportunistic pathogen responsible for various nosocomial infections
Low production of outer membrane protein A (OmpA) in the outer membrane of A. baumannii mutant with Tn-inserted bfmS gene To identify genes controlling OmpA production or localization in the outer membrane, random transposon mutagenesis was performed in A. baumannii ATCC 17978
Two mutant strains (#691 and #692), in which Tn was inserted between nucleotide 954 and 955 in the A1S_0749 gene, exhibited low production of OmpA in the outer membrane as compared to wild-type A. baumannii ATCC 17978 (Fig. 1)
Summary
Acinetobacter baumannii is an important opportunistic pathogen responsible for various nosocomial infections. Acinetobacter baumannii is a clinically important opportunistic pathogen responsible for various nosocomial infections, including ventilator-associated pneumonia, bacteremia, skin and soft tissue infections, urinary tract infections, and meningitis, especially in critically ill patients [1,2,3] Treatment of this microorganism is challenging due to antimicrobial resistance, to carbapenems and colistin [4, 5]. One previous study demonstrated that the BfmS-deficient mutant increasingly released OmpA, TEM-1 β-lactamase, and CarO into the supernatant compared to the wild-type A. baumannii strain [30] This observation suggests that BfmS possibly controls production of OMVs, because a large amount of OmpA in culture supernatant is found in OMVs [13]. The present study was conducted to investigate whether sensor kinase BfmS controls localization of OmpA in either the outer membrane or OMVs, which subsequently affects OMV production, using wild-type A. baumannii ATCC 17978, ΔbfmS mutant, and bfmScomplemented strains
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