<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Scott WC</submitter><funding>NCATS NIH HHS</funding><funding>NIA NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>National Institutes of Health</funding><pagination>1318-1328.e5</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8035132</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>147(4)</volume><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Objective&lt;/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.&lt;h4>Methods&lt;/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</pubmed_abstract><journal>The Journal of allergy and clinical immunology</journal><pubmed_title>Inflammatory heterogeneity in aspirin-exacerbated respiratory disease.</pubmed_title><pmcid>PMC8035132</pmcid><funding_grant_id>R01 AG065550</funding_grant_id><funding_grant_id>K23 AI118804</funding_grant_id><funding_grant_id>R21 AI142321</funding_grant_id><funding_grant_id>UL1 TR000445</funding_grant_id><pubmed_authors>Scott WC</pubmed_authors><pubmed_authors>Chowdhury NI</pubmed_authors><pubmed_authors>Chandra RK</pubmed_authors><pubmed_authors>Cahill KN</pubmed_authors><pubmed_authors>Dennis S</pubmed_authors><pubmed_authors>Snyder J</pubmed_authors><pubmed_authors>Turner JH</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Sheng Q</pubmed_authors><pubmed_authors>Huang LC</pubmed_authors><pubmed_authors>Bauer AM</pubmed_authors><pubmed_authors>Milne GL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Inflammatory heterogeneity in aspirin-exacerbated respiratory disease.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Objective&lt;/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.&lt;h4>Methods&lt;/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</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Apr</publication><modification>2025-04-29T11:31:21.645Z</modification><creation>2025-04-06T19:54:18.593Z</creation></dates><accession>S-EPMC8035132</accession><cross_references><pubmed>33189729</pubmed><doi>10.1016/j.jaci.2020.11.001</doi></cross_references></HashMap>