<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Magrin GL</submitter><funding>Austrian Science Fund FWF</funding><funding>Osteology Foundation</funding><pagination>E1679</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7084181</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(5)</volume><pubmed_abstract>Short-chain fatty acids (SCFA) are bacterial metabolites that can be found in periodontal pockets. The expression of adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) within the epithelium pocket is considered to be a key event for the selective transmigration of leucocytes towards the gingival sulcus. However, the impact of SCFA on ICAM-1 expression by oral epithelial cells remains unclear. We therefore exposed the oral squamous carcinoma cell line HSC-2, primary oral epithelial cells and human gingival fibroblasts to SCFA, namely acetate, propionate and butyrate, and stimulated with known inducers of ICAM-1 such as interleukin-1-beta (IL1β) and tumor necrosis factor-alfa (TNFα). We report here that butyrate but not acetate or propionate significantly suppressed the cytokine-induced ICAM-1 expression in HSC-2 epithelial cells and primary epithelial cells. The G-protein coupled receptor-43 (GPR43/ FFAR2) agonist but not the histone deacetylase inhibitor, trichostatin A, mimicked the butyrate effects. Butyrate also attenuated the nuclear translocation of p65 into the nucleus on HSC-2 cells. The decrease of ICAM-1 was independent of Nrf2/HO-1 signaling and phosphorylation of JNK and p38. Nevertheless, butyrate could not reverse an ongoing cytokine-induced ICAM-1 expression in HSC-2 cells. Overall, these observations suggest that butyrate can attenuate cytokine-induced ICAM-1 expression in cells with epithelial origin.</pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Butyrate Decreases ICAM-1 Expression in Human Oral Squamous Cell Carcinoma Cells.</pubmed_title><pmcid>PMC7084181</pmcid><funding_grant_id>I 4072</funding_grant_id><funding_grant_id>17-125</funding_grant_id><funding_grant_id>4072-B28</funding_grant_id><pubmed_authors>Mildner M</pubmed_authors><pubmed_authors>Di Summa F</pubmed_authors><pubmed_authors>Gruber R</pubmed_authors><pubmed_authors>Magalhaes Benfatti CA</pubmed_authors><pubmed_authors>Magrin GL</pubmed_authors><pubmed_authors>Strauss FJ</pubmed_authors><pubmed_authors>Panahipour L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Butyrate Decreases ICAM-1 Expression in Human Oral Squamous Cell Carcinoma Cells.</name><description>Short-chain fatty acids (SCFA) are bacterial metabolites that can be found in periodontal pockets. The expression of adhesion molecules such as intercellular adhesion molecule-1 (ICAM-1) within the epithelium pocket is considered to be a key event for the selective transmigration of leucocytes towards the gingival sulcus. However, the impact of SCFA on ICAM-1 expression by oral epithelial cells remains unclear. We therefore exposed the oral squamous carcinoma cell line HSC-2, primary oral epithelial cells and human gingival fibroblasts to SCFA, namely acetate, propionate and butyrate, and stimulated with known inducers of ICAM-1 such as interleukin-1-beta (IL1β) and tumor necrosis factor-alfa (TNFα). We report here that butyrate but not acetate or propionate significantly suppressed the cytokine-induced ICAM-1 expression in HSC-2 epithelial cells and primary epithelial cells. The G-protein coupled receptor-43 (GPR43/ FFAR2) agonist but not the histone deacetylase inhibitor, trichostatin A, mimicked the butyrate effects. Butyrate also attenuated the nuclear translocation of p65 into the nucleus on HSC-2 cells. The decrease of ICAM-1 was independent of Nrf2/HO-1 signaling and phosphorylation of JNK and p38. Nevertheless, butyrate could not reverse an ongoing cytokine-induced ICAM-1 expression in HSC-2 cells. Overall, these observations suggest that butyrate can attenuate cytokine-induced ICAM-1 expression in cells with epithelial origin.</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Feb</publication><modification>2024-11-06T13:04:34.057Z</modification><creation>2020-05-22T14:06:49Z</creation></dates><accession>S-EPMC7084181</accession><cross_references><pubmed>32121422</pubmed><doi>10.3390/ijms21051679</doi></cross_references></HashMap>