English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Actinobacillus pleuropneumoniae  (APP) is the major pathogen of porcine contagious pleuropneumoniae (PCP). The QseB/QseC two-component system (TCS) consists of the regulator QseB and the kinase QseC, which relates to quorum sensing (QS) and virulence in some bacteria. Here, we investigated the role of QseB/QseC in  apf  gene cluster ( apfABCD ) expression of APP. Our results have showed that QseB/QseC TCS can potentially regulate the expression of  apf  gene cluster. The Δ qseBC , Δ apfA , Δ apfB , Δ apfC  and Δ apfD  strains are more sensitive to acidic and osmotic stressful conditions, and exhibite lower biofilm formation ability than wild-type (WT) strain, whereas the complemented strains show similar phenotype to the WT strain. In additon, the mutants have defective anti-phagocytosis, adhesion and invasion when they come into contact with the host cells. In experimental animal models of infection, mice infected with Δ qseBC , Δ apfA , Δ apfB , Δ apfC  and Δ apfD  strains showed lower mortality and bacterial loads in the lung and the blood than those infected with WT strain. In conclusion, our results suggest that QseB/QseC TCS contributes to stress resistance, biofilm formation, phagocytosis, adhesion, invasion and virulence by downregulating expression of  apf  gene cluster in  A. pleuropneumoniae .

The QseB/QseC two-component system contributes to virulence of Actinobacillus pleuropneumoniae by downregulating apf gene cluster transcription