{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Nunomura S"],"funding":["NHLBI NIH HHS"],"pagination":["111933"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11486451"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["42(1)"],"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"],"journal":["Cell reports"],"pubmed_title":["Periostin activates distinct modules of inflammation and itching downstream of the type 2 inflammation pathway."],"pmcid":["PMC11486451"],"funding_grant_id":["R01 HL060714","R01 HL148165"],"pubmed_authors":["Nanri Y","Uta D","Ejiri N","Izuhara K","Yamamoto S","Koga M","Nunomura S","Ikemitsu H","Kitajima I","Conway SJ","Takedomi H","Honda Y","Andoh T","Matsuda K","Kitajima M"],"additional_accession":[]},"is_claimable":false,"name":"Periostin activates distinct modules of inflammation and itching downstream of the type 2 inflammation pathway.","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","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-26T13:57:03.591Z","creation":"2025-04-06T14:24:29.185Z"},"accession":"S-EPMC11486451","cross_references":{"pubmed":["36610396"],"doi":["10.1016/j.celrep.2022.111933"]}}