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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.

10′(Z),13′(E)-Heptadecadienylhydroquinone Inhibits Swarming and Virulence Factors and Increases Polymyxin B Susceptibility in Proteus mirabilis