{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Scott WC"],"funding":["NCATS NIH HHS","NIA NIH HHS","NIAID NIH HHS","National Institutes of Health"],"pagination":["1318-1328.e5"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8035132"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["147(4)"],"pubmed_abstract":["<h4>Background</h4>Aspirin-exacerbated respiratory disease (AERD) is a mechanistically distinct subtype of chronic rhinosinusitis with nasal polyps (CRSwNP). Although frequently associated with type 2 inflammation, literature characterizing the milieu of inflammatory cytokines and lipid mediators in AERD has been conflicting.<h4>Objective</h4>We sought to identify differences in the upper airway inflammatory signature between CRSwNP and AERD and determine whether endotypic subtypes of AERD may exist.<h4>Methods</h4>Levels of 7 cytokines representative of type 1, type 2, and type 3 inflammation, and 21 lipid mediators were measured in nasal mucus from 109 patients with CRSwNP, 30 patients with AERD, and 64 non-CRS controls. Differences in inflammatory mediators were identified between group"],"journal":["The Journal of allergy and clinical immunology"],"pubmed_title":["Inflammatory heterogeneity in aspirin-exacerbated respiratory disease."],"pmcid":["PMC8035132"],"funding_grant_id":["R01 AG065550","K23 AI118804","R21 AI142321","UL1 TR000445"],"pubmed_authors":["Scott WC","Chowdhury NI","Chandra RK","Cahill KN","Dennis S","Snyder J","Turner JH","Li P","Sheng Q","Huang LC","Bauer AM","Milne GL"],"additional_accession":[]},"is_claimable":false,"name":"Inflammatory heterogeneity in aspirin-exacerbated respiratory disease.","description":"<h4>Background</h4>Aspirin-exacerbated respiratory disease (AERD) is a mechanistically distinct subtype of chronic rhinosinusitis with nasal polyps (CRSwNP). Although frequently associated with type 2 inflammation, literature characterizing the milieu of inflammatory cytokines and lipid mediators in AERD has been conflicting.<h4>Objective</h4>We sought to identify differences in the upper airway inflammatory signature between CRSwNP and AERD and determine whether endotypic subtypes of AERD may exist.<h4>Methods</h4>Levels of 7 cytokines representative of type 1, type 2, and type 3 inflammation, and 21 lipid mediators were measured in nasal mucus from 109 patients with CRSwNP, 30 patients with AERD, and 64 non-CRS controls. Differences in inflammatory mediators were identified between group","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2025-04-29T11:31:21.645Z","creation":"2025-04-06T19:54:18.593Z"},"accession":"S-EPMC8035132","cross_references":{"pubmed":["33189729"],"doi":["10.1016/j.jaci.2020.11.001"]}}