<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>6(1)</volume><submitter>Gard AL</submitter><funding>Colgate-Palmolive Company</funding><pubmed_abstract>Nearly half of American adults suffer from gum disease, including mild inflammation of gingival tissue, known as gingivitis. Currently, advances in therapeutic treatments are hampered by a lack of mechanistic understanding of disease progression in physiologically relevant vascularized tissues. To address this, we present a high-throughput microfluidic organ-on-chip model of human gingival tissue containing keratinocytes, fibroblast and endothelial cells. We show the triculture model exhibits physiological tissue structure, mucosal barrier formation, and protein biomarker expression and secretion over several weeks. Through inflammatory cytokine administration, we demonstrate the induction of inflammation measured by changes in barrier function and cytokine secretion. These states of infla</pubmed_abstract><journal>Communications biology</journal><pagination>92</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9870913</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A high-throughput, 28-day, microfluidic model of gingival tissue inflammation and recovery.</pubmed_title><pmcid>PMC9870913</pmcid><pubmed_authors>Cooper MH</pubmed_authors><pubmed_authors>Isenberg BC</pubmed_authors><pubmed_authors>Charest JL</pubmed_authors><pubmed_authors>Azizgolshani H</pubmed_authors><pubmed_authors>Luu RJ</pubmed_authors><pubmed_authors>Cain BP</pubmed_authors><pubmed_authors>Gard AL</pubmed_authors><pubmed_authors>Borenstein JT</pubmed_authors><pubmed_authors>Vedula EM</pubmed_authors><pubmed_authors>Maloney R</pubmed_authors><pubmed_authors>Ong J</pubmed_authors></additional><is_claimable>false</is_claimable><name>A high-throughput, 28-day, microfluidic model of gingival tissue inflammation and recovery.</name><description>Nearly half of American adults suffer from gum disease, including mild inflammation of gingival tissue, known as gingivitis. Currently, advances in therapeutic treatments are hampered by a lack of mechanistic understanding of disease progression in physiologically relevant vascularized tissues. To address this, we present a high-throughput microfluidic organ-on-chip model of human gingival tissue containing keratinocytes, fibroblast and endothelial cells. We show the triculture model exhibits physiological tissue structure, mucosal barrier formation, and protein biomarker expression and secretion over several weeks. Through inflammatory cytokine administration, we demonstrate the induction of inflammation measured by changes in barrier function and cytokine secretion. These states of infla</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2026-03-31T11:00:10.885Z</modification><creation>2025-04-07T05:53:31.082Z</creation></dates><accession>S-EPMC9870913</accession><cross_references><pubmed>36690695</pubmed><doi>10.1038/s42003-023-04434-9</doi></cross_references></HashMap>