as QSI than aromatic or polyaromatic compounds. Indeed, solenopsin A, a venom alkaloid produced by the fire ant Solenopsis invicta, has been shown to inhibit biofilm formation, pyocyanin and elastase production as well as the expression of QS-regulated genes lasB, rhlI and lasI in P. aeruginosa. Peters and co-workers also demonstrated that brominated tryptamine-based alkaloids from Flustrafoliacea, a sea bryozoan, inhibit AHL-regulated gene expression using biosensors P. putida, P. putida and E. coli lasR, cepR and luxR coupled to the promoter of lasB, cepI and luxI, respectively. In this study, the QSI activity of human Licochalcone A hormones was supported by complementary features. The pure hormones, especially estriol and estrone, affected expression of the QSregulated reporter fusion traG-lacZ and QS-dependent horizontal transfer of the virulence Ti-plasmid in A. tumefaciens. They also decreased the expression of six QS-regulated genes lasI, lasR, lasB, rhlI, rhlR, and rhlA in P. aeruginosa, but none decreased expression of the QS-independent gene aceA. Because of the effect on lasI and rhlI, the AHL concentration was also affected in the presence of the sexual hormones. In MEDChem Express Compound 401 agreement with a previous report comparing the effect of steroid hormones on the growth of several pathogens, they did not affect the growth of A. tumefaciens and P. aeruginosa at the concentrations used for describing QSI activity. The sexual hormones act as QSIs at a mM-range concentration which is similar to that of the natural polycyclic QSIs such as catechin and naringenin, but higher than that of some other natural and synthetic QSIs which act at a mM range or lower. Our work also revealed that pure hormones affected the QS-regulated reporter gene of P. aeruginosa when RhlR or LasR was expressed in E. coli in the presence of the appropriate AHL. Moreover, molecular modeling confirmed the competitive hormone-binding capacity of the two AHL-sensors LasR and TraR, suggesting that the AHL-LuxR sensor
