Molecular basis of Yersinia enterocolitica temperature-dependent resistance to antimicrobial peptides.

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dc.contributor.author Reinés, Mar
dc.contributor.author Llobet, Enrique
dc.contributor.author Llompart, Catalina M.
dc.contributor.author Moranta Mesquida, David
dc.contributor.author Pérez-Gutiérrez, Camino
dc.contributor.author Bengoechea, José Antonio
dc.date.accessioned 2018-09-14T11:27:46Z
dc.identifier.uri http://hdl.handle.net/11201/147424
dc.description.abstract [eng] Antimicrobial peptides (APs) belong to the arsenal of weapons of the innate immune system against infections. In the case of Gram-negative bacteria, APs interact with the anionic lipid A moiety of the lipopolysaccharide (LPS). In yersiniae most virulence factors are temperature regulated. Studies from our laboratory demonstrated that Yersinia enterocolitica is more susceptible to polymyxin B, a model AP, when grown at 37°C than at 22°C (J. A. Bengoechea, R. Díaz, and I. Moriyón, Infect. Immun. 64:4891-4899, 1996), and here we have extended this observation to other APs, not structurally related to polymyxin B. Mechanistically, we demonstrate that the lipid A modifications with aminoarabinose and palmitate are downregulated at 37°C and that they contribute to AP resistance together with the LPS O-polysaccharide. Bacterial loads of lipid A mutants in Peyer's patches, liver, and spleen of orogastrically infected mice were lower than those of the wild-type strain at 3 and 7 days postinfection. PhoPQ and PmrAB two-component systems govern the expression of the loci required to modify lipid A with aminoarabinose and palmitate, and their expressions are also temperature regulated. Our findings support the notion that the temperature-dependent regulation of loci controlling lipid A modifications could be explained by H-NS-dependent negative regulation alleviated by RovA. In turn, our data also demonstrate that PhoPQ and PmrAB regulate positively the expression of rovA, the effect of PhoPQ being more important. However, rovA expression reached wild-type levels in the phoPQ pmrAB mutant background, hence indicating the existence of an unknown regulatory network controlling rovA expression in this background.
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dc.relation.isformatof Versió postprint del document publicat a: https://doi.org/10.1128/JB.00308-12
dc.relation.ispartof Journal of Bacteriology, 2012, vol. 194, num. 12, p. 3173-3188
dc.subject.classification 579 - Microbiologia
dc.subject.other 579 - Microbiology
dc.title Molecular basis of Yersinia enterocolitica temperature-dependent resistance to antimicrobial peptides.
dc.type info:eu-repo/semantics/article
dc.type info:eu-repo/semantics/acceptedVersion
dc.date.updated 2018-09-14T11:27:46Z
dc.date.embargoEndDate info:eu-repo/date/embargoEnd/2075-01-01
dc.embargo 2075-01-01
dc.rights.accessRights info:eu-repo/semantics/embargoedAccess
dc.identifier.doi https://doi.org/10.1128/JB.00308-12


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