Abstract
Acinetobacter baumannii is an important nosocomial pathogen that can survive in different environmental conditions and poses a severe threat to public health due to its multidrug resistance properties. Research on transcriptional regulators, which play an essential role in adjusting to new environments, could provide new insights into A. baumannii pathogenesis. LysR-type transcriptional regulators (LTTRs) are structurally conserved among bacterial species and regulate virulence in many pathogens. We identified a novel LTTR, designated as LeuO encoded in the A. baumannii genome. After construction of LeuO mutant strain, transcriptome analysis showed that LeuO regulates the expression of 194 upregulated genes and 108 downregulated genes responsible for various functions and our qPCR validation of several differentially expressed genes support transcriptome data. Our results demonstrated that disruption of LeuO led to increased biofilm formation and increased pathogenicity in an animal model. However, the adherence and surface motility of the LeuO mutant were reduced compared with those of the wild-type strain. We observed some mutations on amino acids sequence of LeuO in clinical isolates. These mutations in the A. baumannii biofilm regulator LeuO may cause hyper-biofilm in the tested clinical isolates. This study is the first to demonstrate the association between the LTTR member LeuO and virulence traits of A. baumannii.
Highlights
Acinetobacter baumannii is a member of ESKAPE pathogens that primarily affect patients with compromised defense in hospitals (Rice, 2008)
Because of the differences in some virulence-related traits such as biofilm formation and surface motility, we investigated the in vivo virulence of A. baumannii WT strain, DLeuO strain, and CP strain in a mice infection model
Prokaryotes have diverse transcription factors that regulate gene expression to adjust to new environments, among which the LysR-type transcriptional regulators (LTTRs) family is highly conserved in bacteria (Rivera-Gómez et al, 2011)
Summary
Acinetobacter baumannii is a member of ESKAPE pathogens that primarily affect patients with compromised defense in hospitals (Rice, 2008). Numerous virulence factors contribute to successful A. baumannii infection, including biofilm formation on biological and innate surfaces (Longo et al, 2014), adherence to and invasion. A. baumannii pili are a key factor for biofilm formation, and csuA/ BABCDE chaperone-usher secretion system-mediated pili help planktonic bacteria to adhere onto abiotic surfaces for biofilm formation (Tomaras et al, 2003). A. baumannii can attach onto biotic surfaces such as respiratory epithelial cells, which is another important virulence factor for infection (Lee et al, 2008). Quorum sensing in A. baumannii is another important pathway by which the pathogen senses extracellular signals and regulates biofilm formation and virulence (Bhargava et al, 2015). Understanding the molecular mechanisms of virulence factors would help develop novel strategies to prevent multidrug-resistant A. baumannii infection
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