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dc.contributor.authorRubio-Gómez, José Manuel
dc.contributor.authorMolina Santiago, Carlos Alberto
dc.contributor.authorUdaondo Domínguez, Zulema
dc.contributor.authorTena Garitaonaindia, Mireia 
dc.contributor.authorKrell, Tino
dc.contributor.authorRamos, Juan-Luis
dc.contributor.authorDaddaoua, Abdelali 
dc.date.accessioned2020-03-27T10:57:23Z
dc.date.available2020-03-27T10:57:23Z
dc.date.issued2020-02-20
dc.identifier.citationRubio-Gómez JM, Santiago CM, Udaondo Z, Garitaonaindia MT, Krell T, Ramos J-L and Daddaoua A (2020) Full Transcriptomic Response of Pseudomonas aeruginosa to an Inulin-Derived Fructooligosaccharide. Front. Microbiol. 11:202. [doi: 10.3389/fmicb.2020.00202]es_ES
dc.identifier.urihttp://hdl.handle.net/10481/60727
dc.descriptionThe Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fmicb. 2020.00202/full#supplementary-materiales_ES
dc.description.abstractPseudomonas aeruginosa is an ubiquitous gram-negative opportunistic human pathogen which is not considered part of the human commensal gut microbiota. However, depletion of the intestinal microbiota (Dysbiosis) following antibiotic treatment facilitates the colonization of the intestinal tract by Multidrug-Resistant P. aeruginosa. One possible strategy is based on the use of functional foods with prebiotic activity. The bifidogenic effect of the prebiotic inulin and its hydrolyzed form (fructooligosaccharide: FOS) is well established since they promote the growth of specific beneficial (probiotic) gut bacteria such as bifidobacteria. Previous studies of the opportunistic nosocomial pathogen Pseudomonas aeruginosa PAO1 have shown that inulin and to a greater extent FOS reduce growth and biofilm formation, which was found to be due to a decrease in motility and exotoxin secretion. However, the transcriptional basis for these phenotypic alterations remains unclear. To address this question we conducted RNAsequence analysis. Changes in the transcript level induced by inulin and FOS were similar, but a set of transcript levels were increased in response to inulin and reduced in the presence of FOS. In the presence of inulin or FOS, 260 and 217 transcript levels, respectively, were altered compared to the control to which no polysaccharide was added. Importantly, changes in transcript levels of 57 and 83 genes were found to be specific for either inulin or FOS, respectively, indicating that both compounds trigger different changes. Gene pathway analyses of differentially expressed genes (DEG) revealed a specific FOS-mediated reduction in transcript levels of genes that participate in several canonical pathways involved in metabolism and growth, motility, biofilm formation, b-lactamase resistance, and in the modulation of type III and VI secretion systems; results that have been partially verified by real time quantitative PCR measurements. Moreover, we have identified a genomic island formed by a cluster of 15 genes, encoding uncharacterized proteins, which were repressed in the presence of FOS. The analysis of isogenic mutants has shown that genes of this genomic island encode proteins involved in growth, biofilm formation and motility. These results indicate that FOS selectively modulates bacterial pathogenicity by interfering with different signaling pathways.es_ES
dc.description.sponsorshipThis work was supported by grants from the Spanish Ministry for Economy and Competitiveness (AGL2017-85270-R). CS is funded by the program Juan de la Cierva-Formación (FJCI-2015-23810).es_ES
dc.language.isoenges_ES
dc.publisherFrontiers Mediaes_ES
dc.rightsAtribución 3.0 España*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectRNA sequencinges_ES
dc.subjectrt-qPCRes_ES
dc.subjectAdhesiones_ES
dc.subjectDevelopmental processes_ES
dc.subjectMolecular transduceres_ES
dc.subjectPathogenicityes_ES
dc.titleFull Transcriptomic Response of Pseudomonas aeruginosa to an Inulin-Derived Fructooligosaccharidees_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES
dc.identifier.doi10.3389/fmicb.2020.00202


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Atribución 3.0 España
Except where otherwise noted, this item's license is described as Atribución 3.0 España