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10'-Heptadecadienylhydroquinone Inhibits Swarming and Virulence Factors and Increases Polymyxin B Susceptibility in Proteus mirabilis

Liu, Ming-Che ; Lin, Shwu-Bin ; Chien, Hsiung-Fei ; Wang, Won-Bo ; Yuan, Yu-Han ; Hsueh, Po-Ren ; Liaw, Shwu-Jen

PloS one, 2012-09, Vol.7 (9), p.e45563 [Periódico revisado por pares]

Public Library of Science

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  • Título:
    10'-Heptadecadienylhydroquinone Inhibits Swarming and Virulence Factors and Increases Polymyxin B Susceptibility in Proteus mirabilis
  • Autor: Liu, Ming-Che ; Lin, Shwu-Bin ; Chien, Hsiung-Fei ; Wang, Won-Bo ; Yuan, Yu-Han ; Hsueh, Po-Ren ; Liaw, Shwu-Jen
  • Assuntos: Dosage and administration ; Hemolysis ; Hemolysis and hemolysins ; Polymyxin B ; Toxicodendron
  • É parte de: PloS one, 2012-09, Vol.7 (9), p.e45563
  • Descrição: In this study, we demonstrated that 10'(Z), 13'(E)-heptadecadienylhydroquinone (HQ17-2), isolated from the lacquer tree, could decrease swarming motility and hemolysin activity but increase polymyxin B (PB) susceptibilityof Proteus mirabilis which is intrinsically highly-resistant to PB. The increased PB susceptibility induced by HQ17-2 was also observed in clinical isolates and biofilm-grown cells. HQ17-2 could inhibit swarming in the wild-type and rppA mutant but not in the rcsB mutant, indicating that HQ17-2 inhibits swarming through the RcsB-dependent pathway, a two-component signaling pathway negatively regulating swarming and virulence factor expression. The inhibition of hemolysin activity by HQ17-2 is also mediated through the RcsB-dependent pathway, because HQ17-2 could not inhibit hemolysin activity in the rcsB mutant. Moreover, the finding that HQ17-2 inhibits the expression of flhDC gene in the wild-type and rcsB-complemented strain but not in the rcsB mutant supports the notion. By contrast, HQ17-2 could increase PB susceptibility in the wild-type and rcsB mutant but not in the rppA mutant, indicating that HQ17-2 increases PB susceptibility through the RppA-dependent pathway, a signaling pathway positively regulating PB resistance. In addition, HQ17-2 could inhibit the promoter activities of rppA and pmrI, a gene positively regulated by RppA and involved in PB resistance, in the wild-type but not in the rppA mutant. The inhibition of rppA and pmrI expression caused lipopolysaccharide purified from HQ17-2-treated cells to have higher affinity for PB. Altogether, this study uncovers new biological effects of HQ17-2 and provides evidence for the potential of HQ17-2 in clinical applications.
  • Editor: Public Library of Science
  • Idioma: Inglês
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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