<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Chan H</submitter><funding>NIDDK NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>NIAMS NIH HHS</funding><pagination>eads0519</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12183641</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(106)</volume><pubmed_abstract>Infections after psychological stress are a major health care problem. Single-cell transcriptomics and lipidomic profiling in a mouse model of stress show that dermal fibroblasts undergoing adipogenesis have defective responses to &lt;i>Staphylococcus aureus&lt;/i> skin infection. Adrenalectomy or adrenergic inhibition restores the fibroblast adipogenic response to &lt;i>S. aureus&lt;/i> and enables mice to effectively resist infection during stress. Increased susceptibility to &lt;i>S. aureus&lt;/i> from stress is attributed to suppression of the antimicrobial peptide cathelicidin (&lt;i>Camp&lt;/i>) because adrenaline directly inhibits &lt;i>Camp&lt;/i> production by fibroblasts, and mice lacking &lt;i>Camp&lt;/i> in fibroblasts do not increase infection after stress. Transforming growth factor β (TGFβ) is induced by stres</pubmed_abstract><journal>Science immunology</journal><pubmed_title>Psychological stress increases skin infection through the action of TGFβ to suppress immune-acting fibroblasts.</pubmed_title><pmcid>PMC12183641</pmcid><funding_grant_id>P50 AR080594</funding_grant_id><funding_grant_id>R01 DK128787</funding_grant_id><funding_grant_id>U01 AI152038</funding_grant_id><funding_grant_id>R37 AI052453</funding_grant_id><funding_grant_id>R01 AI168005</funding_grant_id><pubmed_authors>Chan H</pubmed_authors><pubmed_authors>Nakatsuji T</pubmed_authors><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Dokoshi T</pubmed_authors><pubmed_authors>Crown B</pubmed_authors><pubmed_authors>Chiu IM</pubmed_authors><pubmed_authors>Gallo RL</pubmed_authors><pubmed_authors>Li F</pubmed_authors><pubmed_authors>Cavagnero KJ</pubmed_authors><pubmed_authors>Li Q</pubmed_authors><pubmed_authors>Yang D</pubmed_authors><pubmed_authors>Williams KJ</pubmed_authors><pubmed_authors>Aguilera C</pubmed_authors><pubmed_authors>Bensinger SJ</pubmed_authors><pubmed_authors>Chen W</pubmed_authors><pubmed_authors>Valentina O</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Liu E</pubmed_authors><pubmed_authors>Indra A</pubmed_authors><pubmed_authors>Numata T</pubmed_authors></additional><is_claimable>false</is_claimable><name>Psychological stress increases skin infection through the action of TGFβ to suppress immune-acting fibroblasts.</name><description>Infections after psychological stress are a major health care problem. Single-cell transcriptomics and lipidomic profiling in a mouse model of stress show that dermal fibroblasts undergoing adipogenesis have defective responses to &lt;i>Staphylococcus aureus&lt;/i> skin infection. Adrenalectomy or adrenergic inhibition restores the fibroblast adipogenic response to &lt;i>S. aureus&lt;/i> and enables mice to effectively resist infection during stress. Increased susceptibility to &lt;i>S. aureus&lt;/i> from stress is attributed to suppression of the antimicrobial peptide cathelicidin (&lt;i>Camp&lt;/i>) because adrenaline directly inhibits &lt;i>Camp&lt;/i> production by fibroblasts, and mice lacking &lt;i>Camp&lt;/i> in fibroblasts do not increase infection after stress. Transforming growth factor β (TGFβ) is induced by stres</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Apr</publication><modification>2026-06-03T07:10:44.236Z</modification><creation>2026-04-25T03:22:41.312Z</creation></dates><accession>S-EPMC12183641</accession><cross_references><pubmed>40215323</pubmed><doi>10.1126/sciimmunol.ads0519</doi></cross_references></HashMap>