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Stenotrophomonas maltophilia , a gram-negative bacterium, has increasingly emerged as an important nosocomial pathogen. It is well-known for resistance to a variety of antimicrobial agents including cationic antimicrobial polypeptides (CAPs). Resistance to polymyxin B, a kind of CAPs, is known to be controlled by the two-component system PhoPQ. To unravel the role of PhoPQ in polymyxin B resistance of  S .  maltophilia , a  phoP  mutant was constructed. We found MICs of polymyxin B, chloramphenicol, ampicillin, gentamicin, kanamycin, streptomycin and spectinomycin decreased 2–64 fold in the  phoP  mutant. Complementation of the  phoP  mutant by the wild-type  phoP  gene restored all of the MICs to the wild type levels. Expression of PhoP was shown to be autoregulated and responsive to Mg 2+  levels. The polymyxin B and gentamicin killing tests indicated that pretreatment of low Mg 2+  can protect the wild-type  S .  maltophilia  from killing but not  phoP  mutant. Interestingly, we found  phoP  mutant had a decrease in expression of SmeZ, an efflux transporter protein for aminoglycosides in  S .  maltophilia . Moreover,  phoP  mutant showed increased permeability in the cell membrane relative to the wild-type. In summary, we demonstrated the two-component regulator PhoP of  S .  maltophilia  is involved in antimicrobial susceptibilities and low Mg 2+  serves as a signal for triggering the pathway. Both the alteration in membrane permeability and downregulation of SmeZ efflux transporter in the  phoP  mutant contributed to the increased drug susceptibilities of  S .  maltophilia , in particular for aminoglycosides. This is the first report to describe the role of the Mg 2+ -sensing PhoP signaling pathway of  S .  maltophilia  in regulation of the SmeZ efflux transporter and in antimicrobial susceptibilities. This study suggests PhoPQ TCS may serve as a target for development of antimicrobial agents against multidrug-resistant  S .  maltophilia .

Stenotrophomonas maltophilia PhoP, a Two-Component Response Regulator, Involved in Antimicrobial Susceptibilities