Sökning: onr:"swepub:oai:prod.swepub.kib.ki.se:141655988" > Molecular profiling...
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000 | 03061naa a2200517 4500 | |
001 | oai:prod.swepub.kib.ki.se:141655988 | |
003 | SwePub | |
008 | 240916s2019 | |||||||||||000 ||eng| | |
024 | 7 | a http://kipublications.ki.se/Default.aspx?queryparsed=id:1416559882 URI |
024 | 7 | a https://doi.org/10.1038/s41467-019-11722-82 DOI |
040 | a (SwePub)ki | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Thanert, R4 aut |
245 | 1 0 | a Molecular profiling of tissue biopsies reveals unique signatures associated with streptococcal necrotizing soft tissue infections |
264 | c 2019-08-26 | |
264 | 1 | b Springer Science and Business Media LLC,c 2019 |
520 | a Necrotizing soft tissue infections (NSTIs) are devastating infections caused by either a single pathogen, predominantly Streptococcus pyogenes, or by multiple bacterial species. A better understanding of the pathogenic mechanisms underlying these different NSTI types could facilitate faster diagnostic and more effective therapeutic strategies. Here, we integrate microbial community profiling with host and pathogen(s) transcriptional analysis in patient biopsies to dissect the pathophysiology of streptococcal and polymicrobial NSTIs. We observe that the pathogenicity of polymicrobial communities is mediated by synergistic interactions between community members, fueling a cycle of bacterial colonization and inflammatory tissue destruction. In S. pyogenes NSTIs, expression of specialized virulence factors underlies infection pathophysiology. Furthermore, we identify a strong interferon-related response specific to S. pyogenes NSTIs that could be exploited as a potential diagnostic biomarker. Our study provides insights into the pathophysiology of mono- and polymicrobial NSTIs and highlights the potential of host-derived signatures for microbial diagnosis of NSTIs. | |
700 | 1 | a Itzek, A4 aut |
700 | 1 | a Hossmann, J4 aut |
700 | 1 | a Hamisch, D4 aut |
700 | 1 | a Madsen, MB4 aut |
700 | 1 | a Hyldegaard, O4 aut |
700 | 1 | a Skrede, S4 aut |
700 | 1 | a Bruun, T4 aut |
700 | 1 | a Norrby-Teglund, Au Karolinska Institutet4 aut |
700 | 1 | a Medina, E4 aut |
700 | 1 | a Pieper, DH4 aut |
700 | 1 | a Oppegaard, O4 aut |
700 | 1 | a Rath, E4 aut |
700 | 1 | a Nedrebo, T4 aut |
700 | 1 | a Arnell, P4 aut |
700 | 1 | a Rosen, A4 aut |
700 | 1 | a Polzik, P4 aut |
700 | 1 | a Hansen, MB4 aut |
700 | 1 | a Svensson, Mu Karolinska Institutet4 aut |
700 | 1 | a Snall, Ju Karolinska Institutet4 aut |
700 | 1 | a Karlsson, Y4 aut |
700 | 1 | a Nekludov, Mu Karolinska Institutet4 aut |
710 | 2 | a Karolinska Institutet4 org |
773 | 0 | t Nature communicationsd : Springer Science and Business Media LLCg 10:1, s. 3846-q 10:1<3846-x 2041-1723 |
856 | 4 | u https://www.nature.com/articles/s41467-019-11722-8.pdf |
856 | 4 8 | u http://kipublications.ki.se/Default.aspx?queryparsed=id:141655988 |
856 | 4 8 | u https://doi.org/10.1038/s41467-019-11722-8 |
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