The heme sensing response regulator HssR in <Emphasis Type="Italic">Staphylococcus aureus</Emphasis> but not the homologous RR23 in <Emphasis Type="Italic">Listeria monocytogenes</Emphasis> modulates susceptibility to the antimicrobial peptide plectasin |
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| Authors: | Line E Thomsen Caroline T Gottlieb Sanne Gottschalk Tim T Wodskou Hans-Henrik Kristensen Lone Gram Hanne Ingmer |
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| Institution: | 1.Department of Veterinary Disease Biology,University of Copenhagen,Frederiksberg C,Denmark;2.National Institute of Aquatic Resources,Technical University of Denmark,Kgs. Lyngby;3.NovoNordisk,Bagsvaerd,Denmark;4.Novozymes A/S,Bagsvaerd,Denmark;5.Chr. Hansen A/S,Hoersholm,Denmark |
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| Abstract: | Background Host defence peptides (HDPs), also known as antimicrobial peptides (AMPs), have emerged as potential new therapeutics and
their antimicrobial spectrum covers a wide range of target organisms. However, the mode of action and the genetics behind
the bacterial response to HDPs is incompletely understood and such knowledge is required to evaluate their potential as antimicrobial
therapeutics. Plectasin is a recently discovered HDP active against Gram-positive bacteria with the human pathogen, Staphylococcus aureus (S. aureus) being highly susceptible and the food borne pathogen, Listeria monocytogenes (L. monocytogenes) being less sensitive. In the present study we aimed to use transposon mutagenesis to determine the genetic basis for S. aureus and L. monocytogenes susceptibility to plectasin. |
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