<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nunomura S</submitter><funding>NHLBI NIH HHS</funding><pagination>111933</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11486451</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>42(1)</volume><pubmed_abstract>Atopic dermatitis (AD) is a chronic relapsing skin disease accompanied by recurrent itching. Although type 2 inflammation is dominant in allergic skin inflammation, it is not fully understood how non-type 2 inflammation co-exists with type 2 inflammation or how type 2 inflammation causes itching. We have recently established the FADS mouse, a mouse model of AD. In FADS mice, either genetic disruption or pharmacological inhibition of periostin, a downstream molecule of type 2 inflammation, inhibits NF-κB activation in keratinocytes, leading to downregulating eczema, epidermal hyperplasia, and infiltration of neutrophils, without regulating the enhanced type 2 inflammation. Moreover, inhibition of periostin blocks spontaneous firing of superficial dorsal horn neurons followed by a decrease i</pubmed_abstract><journal>Cell reports</journal><pubmed_title>Periostin activates distinct modules of inflammation and itching downstream of the type 2 inflammation pathway.</pubmed_title><pmcid>PMC11486451</pmcid><funding_grant_id>R01 HL060714</funding_grant_id><funding_grant_id>R01 HL148165</funding_grant_id><pubmed_authors>Nanri Y</pubmed_authors><pubmed_authors>Uta D</pubmed_authors><pubmed_authors>Ejiri N</pubmed_authors><pubmed_authors>Izuhara K</pubmed_authors><pubmed_authors>Yamamoto S</pubmed_authors><pubmed_authors>Koga M</pubmed_authors><pubmed_authors>Nunomura S</pubmed_authors><pubmed_authors>Ikemitsu H</pubmed_authors><pubmed_authors>Kitajima I</pubmed_authors><pubmed_authors>Conway SJ</pubmed_authors><pubmed_authors>Takedomi H</pubmed_authors><pubmed_authors>Honda Y</pubmed_authors><pubmed_authors>Andoh T</pubmed_authors><pubmed_authors>Matsuda K</pubmed_authors><pubmed_authors>Kitajima M</pubmed_authors></additional><is_claimable>false</is_claimable><name>Periostin activates distinct modules of inflammation and itching downstream of the type 2 inflammation pathway.</name><description>Atopic dermatitis (AD) is a chronic relapsing skin disease accompanied by recurrent itching. Although type 2 inflammation is dominant in allergic skin inflammation, it is not fully understood how non-type 2 inflammation co-exists with type 2 inflammation or how type 2 inflammation causes itching. We have recently established the FADS mouse, a mouse model of AD. In FADS mice, either genetic disruption or pharmacological inhibition of periostin, a downstream molecule of type 2 inflammation, inhibits NF-κB activation in keratinocytes, leading to downregulating eczema, epidermal hyperplasia, and infiltration of neutrophils, without regulating the enhanced type 2 inflammation. Moreover, inhibition of periostin blocks spontaneous firing of superficial dorsal horn neurons followed by a decrease i</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Jan</publication><modification>2025-04-26T13:57:03.591Z</modification><creation>2025-04-06T14:24:29.185Z</creation></dates><accession>S-EPMC11486451</accession><cross_references><pubmed>36610396</pubmed><doi>10.1016/j.celrep.2022.111933</doi></cross_references></HashMap>