RNA-seq-based transcriptomic analysis of AHL-induced biofilm and pyocyanin inhibition in Pseudomonas aeruginosa by Lactobacillus brevis
Quorum sensing (QS) regulates hundreds of genes in Pseudomonas aeruginosa, and many of which encode extracellular virulence factors. Lactobacillus as a probiotic has been verified to inhibit pathogenesis in P. aeruginosa via quenching QS. The objective of this study was to investigate mechanism of t...
Gespeichert in:
Veröffentlicht in: | International microbiology 2022-08, Vol.25 (3), p.447-456 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Quorum sensing (QS) regulates hundreds of genes in
Pseudomonas aeruginosa,
and many of which encode extracellular virulence factors.
Lactobacillus
as a probiotic has been verified to inhibit pathogenesis in
P. aeruginosa
via quenching QS. The objective of this study was to investigate mechanism of the QS quenching function of
Lactobacillus
via analyzing the gene expression by transcriptome. We previously isolated a
Lactobacillus brevis
strain 3M004 from an aquafeed and identified the strain has the function of degrading QS molecular AHL (OC12-HSL). The result showed that 3M004 cells/lysate inhibited biofilm and pyocyanin production of
P. aeruginosa
PA002. The biofilm inhibition rates were 16.92% and 33.0% after treatment by 1 and 2 mg/mL 3M004 lysate, respectively, and the rates for pyocyanin inhibition were 25.16% and 30.75%, respectively. Transcriptomic analysis showed that down-regulation of genes of
LasA
and
LasB
in PA002 was essential in regulating the QS system. The biofilm decrease of PA002 seems not only resulted from gene biosynthesizing of polysaccharides but also from other genes regulating components biosynthesis. Pyocyanin biosynthesis appears to be inhibited by down-regulating the key gene of
PhzAB
on the nonreversing action from chorismite to pyocyanin. |
---|---|
ISSN: | 1618-1905 1139-6709 1618-1905 |
DOI: | 10.1007/s10123-021-00228-3 |