<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Arjunan P</submitter><funding>NIDCR NIH HHS</funding><funding>National Institutes of Health/NIDCR</funding><pagination>78-93</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5486950</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>31(1)</volume><pubmed_abstract>The human microbiome consists of highly diverse microbial communities that colonize our skin and mucosal surfaces, aiding in maintenance of immune homeostasis. The keystone pathogen Porphyromonas gingivalis induces a dysbiosis and disrupts immune homeostasis through as yet unclear mechanisms. The fimbrial adhesins of P. gingivalis facilitate biofilm formation, invasion of and dissemination by blood dendritic cells; hence, fimbriae may be key factors in disruption of immune homeostasis. In this study we employed RNA-sequencing transcriptome profiling to identify differentially expressed genes (DEGs) in human monocyte-derived dendritic cells (MoDCs) in response to in vitro infection/exposure by Pg381 or its isogenic mutant strains that solely express minor-Mfa1 fimbriae (DPG3), major-FimA fi</pubmed_abstract><journal>Molecular oral microbiology</journal><pubmed_title>High-throughput sequencing reveals key genes and immune homeostatic pathways activated in myeloid dendritic cells by Porphyromonas gingivalis 381 and its fimbrial mutants.</pubmed_title><pmcid>PMC5486950</pmcid><funding_grant_id>R01 DE014328</funding_grant_id><funding_grant_id>R01 DE14328-09</funding_grant_id><funding_grant_id>RO1 DE14328-09</funding_grant_id><funding_grant_id>R21 DE020916</funding_grant_id><funding_grant_id>F31 DE020014</funding_grant_id><pubmed_authors>El-Awady A</pubmed_authors><pubmed_authors>Kunde-Ramamoorthy G</pubmed_authors><pubmed_authors>Arjunan P</pubmed_authors><pubmed_authors>Cutler CW</pubmed_authors><pubmed_authors>Dannebaum RO</pubmed_authors></additional><is_claimable>false</is_claimable><name>High-throughput sequencing reveals key genes and immune homeostatic pathways activated in myeloid dendritic cells by Porphyromonas gingivalis 381 and its fimbrial mutants.</name><description>The human microbiome consists of highly diverse microbial communities that colonize our skin and mucosal surfaces, aiding in maintenance of immune homeostasis. The keystone pathogen Porphyromonas gingivalis induces a dysbiosis and disrupts immune homeostasis through as yet unclear mechanisms. The fimbrial adhesins of P. gingivalis facilitate biofilm formation, invasion of and dissemination by blood dendritic cells; hence, fimbriae may be key factors in disruption of immune homeostasis. In this study we employed RNA-sequencing transcriptome profiling to identify differentially expressed genes (DEGs) in human monocyte-derived dendritic cells (MoDCs) in response to in vitro infection/exposure by Pg381 or its isogenic mutant strains that solely express minor-Mfa1 fimbriae (DPG3), major-FimA fi</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Feb</publication><modification>2026-04-14T09:20:08.722Z</modification><creation>2019-03-27T02:48:38Z</creation></dates><accession>S-EPMC5486950</accession><cross_references><pubmed>26466817</pubmed><doi>10.1111/omi.12131</doi></cross_references></HashMap>