Multiple resistance factors collectively promote inoculum-dependent dynamic survival during antimicrobial peptide exposure in Enterobacter cloacae
Fig 7
Model of Enterobacter cloacae cecropin B dynamic survival.
(A) Mechanisms of AMP resistance discussed in this study. 1) OM stress induces the Rcs phosphorelay, which phosphorylates the response regulator RcsB. Among other systems, RcsB upregulates capsule production. 2) AMPs and envelope stress induces the PhoPQ signaling system, which upregulates transcription of enzymes which modify the outer membrane. 3) OmpT, bound in the outer membrane, may be able to cleave AMPs before they act on the cell surface. (B) Model of E. cloacae growth vs concentration of cecB over time. Black line represents hypothetical population density (indicated by OD600), solid red line represents the hypothetical concentration of cecropin in the sample, and the dotted red line represents the hypothetical concentration of cecropin necessary for lysis. In this model, the population must bring the amount of cecropin below the effective killing concentration before all cells in the population are lysed. Factors like initial starting concentration or protease production may modify the rate at which bacteria can reduce cecropin concentration, while other factors like PhoPQ and RcsB may raise the concentration of cecropin necessary for lysis.