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dc.contributor.authorPekmezovic, Marina
dc.contributor.authorHovhannisyan, Hrant
dc.contributor.authorGresnigt, Mark S.
dc.contributor.authorIracane, Elise
dc.contributor.authorOliveira Pacheco, João
dc.contributor.authorSiscar Lewin, Sofía
dc.contributor.authorSeemann, Eric
dc.contributor.authorQualmann, Britta
dc.contributor.authorKalkreuter, Till
dc.contributor.authorMüller, Sylvia
dc.contributor.authorKamradt, Thomas
dc.contributor.authorMogavero, Selene
dc.contributor.authorBrunke, Sascha
dc.contributor.authorButler, Geraldine
dc.contributor.authorGabaldón, Toni
dc.contributor.authorHube, Bernhard
dc.contributor.otherBarcelona Supercomputing Center
dc.date.accessioned2021-04-19T09:44:14Z
dc.date.issued2021
dc.identifier.citationPekmezovic, M. [et al.]. Candida pathogens induce protective mitochondria-associated type I interferon signalling and a damage-driven response in vaginal epithelial cells. "Nature Microbiology", 2021,
dc.identifier.issn2058-5276
dc.identifier.urihttp://hdl.handle.net/2117/343867
dc.description.abstractVaginal candidiasis is an extremely common disease predominantly caused by four phylogenetically diverse species: Candida albicans; Candida glabrata; Candida parapsilosis; and Candida tropicalis. Using a time course infection model of vaginal epithelial cells and dual RNA sequencing, we show that these species exhibit distinct pathogenicity patterns, which are defined by highly species-specific transcriptional profiles during infection of vaginal epithelial cells. In contrast, host cells exhibit a homogeneous response to all species at the early stages of infection, which is characterized by sublethal mitochondrial signalling inducing a protective type I interferon response. At the later stages, the transcriptional response of the host diverges in a species-dependent manner. This divergence is primarily driven by the extent of epithelial damage elicited by species-specific mechanisms, such as secretion of the toxin candidalysin by C. albicans. Our results uncover a dynamic, biphasic response of vaginal epithelial cells to Candida species, which is characterized by protective mitochondria-associated type I interferon signalling and a species-specific damage-driven response.
dc.description.sponsorshipM.P., H.H., E.I., J.O.P., T.G., G.B. and B.H. received funding from the European Union Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant no. 642095 (OPATHY). B.H. also received support from the German Research Foundation within the Collaborative Research Centre/Transregio 124 FungiNet (project C1). M.S.G. was supported by the German Research Foundation Emmy Noether Programme (project no. 434385622/GR 5617/1-1). We acknowledge the support of the Spanish Ministry of Science, Innovation and Universities (grant no. PGC2018-099921-B-I00) to the European Molecular Biology Laboratory partnership, the Centro de Excelencia Severo Ochoa and the CERCA Programme/Generalitat de Catalunya. We thank C. Kämnitz from the Electron Microscopy Center in Jena for the sample preparation for TEM. The schematic models in Figs. 4–6 were created with images adapted from Servier Medical Art (Servier).
dc.language.isoeng
dc.publisherSpringer Nature
dc.subjectÀrees temàtiques de la UPC::Informàtica::Aplicacions de la informàtica::Bioinformàtica
dc.subject.lcshCandida albicans
dc.subject.lcshEpithelial cells
dc.subject.lcshCandidiasis, Vulvovaginal
dc.subject.otherFungal host response
dc.subject.otherFungal pathogenesis
dc.subject.otherInnate immunity
dc.subject.otherTranscriptomics
dc.titleCandida pathogens induce protective mitochondria-associated type I interferon signalling and a damage-driven response in vaginal epithelial cells
dc.typeArticle
dc.subject.lemacCèl·lules -- Biologia
dc.identifier.doi10.1038/s41564-021-00875-2
dc.description.peerreviewedPeer Reviewed
dc.relation.publisherversionhttps://www.nature.com/articles/s41564-021-00875-2
dc.rights.accessRestricted access - publisher's policy
dc.description.versionPostprint (author's final draft)
dc.date.lift2021-09-22
local.citation.publicationNameNature Microbiology


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