title: Panax ginseng has anti-infective activity against opportunistic pathogen Pseudomonas aeruginosa by inhibiting quorum sensing, a bacterial communication process critical for establishing infection.
abstract: Virulent factors produced by pathogens play an important role in the infectious process, which is regulated by a cell-to-cell communication mechanism called quorum sensing (QS). Pseudomonas aeruginosa is an important opportunistic human pathogen, which causes infections in patients with compromised immune systems and cystic fibrosis. The QS systems of P. aeruginosa use N-acylated homoserine lactone (AHL) as signal molecules. Previously we have demonstrated that Panax ginseng treatment allowed the animals with P. aeruginosa pneumonia to effectively clear the bacterial infection. We postulated that the ability to impact the outcome of infections is partly due to ginseng having direct effect on the production of P. aeruginosa virulence factors. The study explores the effect of ginseng on alginate, protease and AHL production. The effect of ginseng extracts on growth and expression of QS-controlled virulence factors on the prototypic P. aeruginosa PAO1 and its isogenic mucoid variant (PAOmucA22) was determined. Ginseng did not inhibit the growth of the bacteria, enhanced the extracellular protein production and stimulated the production of alginate. However, ginseng suppressed the production of LasA and LasB and down-regulated the synthesis of the AHL molecules. Ginseng has a negative effect on the QS system of P. aeruginosa, may explain the ginseng-dependent bacterial clearance from the animal lungs in vivo in our previous animal study. It is possible that enhancing and repressing activities of ginseng are mutually exclusive as it is a complex mixture, as shown with the HPLC analysis of the hot water extract. Though ginseng is a promising natural synergetic remedy, it is important to isolate and evaluate the ginseng compounds associated with the anti-QS activity.
authors.affiliation: Department of Biological Sciences, College of Arts and Sciences, Florida International University, Miami, FL 33199, USA.
authors.forename: Z
authors.initials: Z
authors.lastname: Song
authors.forename: K F
authors.initials: KF
authors.lastname: Kong
authors.forename: H
authors.initials: H
authors.lastname: Wu
authors.forename: N
authors.initials: N
authors.lastname: Maricic
authors.forename: B
authors.initials: B
authors.lastname: Ramalingam
authors.forename: H
authors.initials: H
authors.lastname: Priestap
authors.forename: L
authors.initials: L
authors.lastname: Schneper
authors.forename: J M E
authors.initials: JM
authors.lastname: Quirke
authors.forename: N
authors.initials: N
authors.lastname: Høiby
authors.forename: K
authors.initials: K
authors.lastname: Mathee
mesh_terms: D015107:4-Butyrolactone / Q000031:analogs & derivatives / Q000096:biosynthesis; D000464:Alginates; D000890:Anti-Infective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001426:Bacterial Proteins / Q000096:biosynthesis*; D002851:Chromatography, High Pressure Liquid; D015536:Down-Regulation; D020723:Glucuronic Acid / Q000096:biosynthesis; D006603:Hexuronic Acids; D008666:Metalloendopeptidases / Q000096:biosynthesis; D005894:Panax; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology*; D011552:Pseudomonas Infections / Q000188:drug therapy* / Q000382:microbiology; D011550:Pseudomonas aeruginosa / Q000187:drug effects* / Q000378:metabolism / Q000472:pathogenicity; D015398:Signal Transduction; D014774:Virulence / Q000187:drug effects; D037521:Virulence Factors / Q000096:biosynthesis*
chemical_list: D000464:Alginates; D000890:Anti-Infective Agents; D001426:Bacterial Proteins; D006603:Hexuronic Acids; D010936:Plant Extracts; D037521:Virulence Factors; C088386:homoserine lactone; D020723:Glucuronic Acid; D008666:Metalloendopeptidases; D015107:4-Butyrolactone