<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ikeda K</submitter><funding>UCB Japan</funding><funding>Eli Lilly (Japan)</funding><funding>Health Labour Sciences Research Grant</funding><funding>Mishima Kaiun Memorial Foundation</funding><funding>Kawasaki Medical School</funding><funding>Japan Society for the Promotion of Science</funding><pagination>4312</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9032572</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(8)</volume><pubmed_abstract>Patients with psoriasis are frequently complicated with metabolic syndrome; however, it is not fully understood how obesity and dyslipidemia contribute to the pathogenesis of psoriasis. To investigate the mechanisms by which obesity and dyslipidemia exacerbate psoriasis using murine models and neonatal human epidermal keratinocytes (NHEKs), we used wild-type and &lt;i>Apoe&lt;/i>-deficient dyslipidemic mice, and administered a high-fat diet for 10 weeks to induce obesity. Imiquimod was applied to the ear for 5 days to induce psoriatic dermatitis. To examine the innate immune responses of NHEKs, we cultured and stimulated NHEKs using IL-17A, TNF-α, palmitic acid, and leptin. We found that obesity and dyslipidemia synergistically aggravated psoriatic dermatitis associated with increased gene expre</pubmed_abstract><journal>International journal of molecular sciences</journal><pubmed_title>Obesity and Dyslipidemia Synergistically Exacerbate Psoriatic Skin Inflammation.</pubmed_title><pmcid>PMC9032572</pmcid><funding_grant_id>N/A</funding_grant_id><funding_grant_id>20K17442</funding_grant_id><funding_grant_id>Eli Lilly Japan KK Research Grant 2021</funding_grant_id><funding_grant_id>21K08484</funding_grant_id><funding_grant_id>R03B-046</funding_grant_id><funding_grant_id>20K08672</funding_grant_id><funding_grant_id>20FC1047</funding_grant_id><pubmed_authors>Ikeda K</pubmed_authors><pubmed_authors>Yahagi A</pubmed_authors><pubmed_authors>Hiramatsu-Asano S</pubmed_authors><pubmed_authors>Iseki M</pubmed_authors><pubmed_authors>Ishihara K</pubmed_authors><pubmed_authors>Tachibana K</pubmed_authors><pubmed_authors>Mukai T</pubmed_authors><pubmed_authors>Wada J</pubmed_authors><pubmed_authors>Morizane S</pubmed_authors><pubmed_authors>Morita Y</pubmed_authors><pubmed_authors>Akagi T</pubmed_authors><pubmed_authors>Kaneto H</pubmed_authors></additional><is_claimable>false</is_claimable><name>Obesity and Dyslipidemia Synergistically Exacerbate Psoriatic Skin Inflammation.</name><description>Patients with psoriasis are frequently complicated with metabolic syndrome; however, it is not fully understood how obesity and dyslipidemia contribute to the pathogenesis of psoriasis. To investigate the mechanisms by which obesity and dyslipidemia exacerbate psoriasis using murine models and neonatal human epidermal keratinocytes (NHEKs), we used wild-type and &lt;i>Apoe&lt;/i>-deficient dyslipidemic mice, and administered a high-fat diet for 10 weeks to induce obesity. Imiquimod was applied to the ear for 5 days to induce psoriatic dermatitis. To examine the innate immune responses of NHEKs, we cultured and stimulated NHEKs using IL-17A, TNF-α, palmitic acid, and leptin. We found that obesity and dyslipidemia synergistically aggravated psoriatic dermatitis associated with increased gene expre</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2025-04-22T03:55:33.604Z</modification><creation>2025-04-05T20:49:45.208Z</creation></dates><accession>S-EPMC9032572</accession><cross_references><pubmed>35457132</pubmed><doi>10.3390/ijms23084312</doi></cross_references></HashMap>