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

Background   Staphylococcus aureus  and  Pseudomonas aeruginosa  are often found together in the airways of cystic fibrosis (CF) patients. It was previously shown that the  P. aeruginosa  exoproduct 4-hydroxy-2-heptylquinoline- N- oxide (HQNO) suppresses the growth of  S. aureus  and provokes the emergence of small-colony variants (SCVs). The presence of  S. aureus  SCVs as well as biofilms have both been associated with chronic infections in CF.    Results  We demonstrated that HQNO stimulates  S. aureus  to form a biofilm in association with the formation of SCVs. The emergence of SCVs and biofilm production under HQNO exposure was shown to be dependent on the activity of the stress- and colonization-related alternative sigma factor B (SigB). Analysis of gene expression revealed that exposure of a prototypical  S. aureus  strain to HQNO activates SigB, which was leading to an increase in the expression of the fibronectin-binding protein A and the biofilm-associated  sarA  genes. Conversely, the quorum sensing accessory gene regulator ( agr ) system and the α-hemolysin gene were repressed by HQNO. Experiments using culture supernatants from  P. aeruginosa  PAO1 and a double chamber co-culture model confirmed that  P. aeruginosa  stimulates biofilm formation and activates SigB in a  S. aureus  strain isolated from a CF patient. Furthermore, the supernatant from  P. aeruginosa  mutants unable to produce HQNO induced the production of biofilms by  S. aureus  to a lesser extent than the wild-type strain only in a  S. aureus  SigB-functional background.    Conclusions  These results suggest that  S. aureus  responds to HQNO from  P. aeruginosa  by forming SCVs and biofilms through SigB activation, a phenomenon that may contribute to the establishment of chronic infections in CF patients.

bmc microbiology

Staphylococcus aureus sigma B-dependent emergence of small-colony variants and biofilm production following exposure to Pseudomonas aeruginosa 4-hydroxy-2-heptylquinoline-N- oxide