{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["De Sadeleer LJ"],"funding":["Stichting Tegen Kanker","NCATS NIH HHS","NHLBI NIH HHS","Three Lakes Partners","Parker B. Francis Foundation","NIH","Fonds National de la Recherche Scientifique – FNRS","Canadian Institutes of Health Research","CIHR","Providence Health Care","KU Leuven","U.S. Department of Defense","Fonds Wetenschappelijk Onderzoek","Michael Smith Foundation for Health Research","NLM NIH HHS","NIH HHS"],"pagination":["60-74"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8865586"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["205(1)"],"pubmed_abstract":["<b>Rationale:</b> Fibrotic hypersensitivity pneumonitis (fHP) is an interstitial lung disease caused by sensitization to an inhaled allergen. <b>Objectives:</b> To identify the molecular determinants associated with progression of fibrosis. <b>Methods:</b> Nine fHP explant lungs and six unused donor lungs (as controls) were systematically sampled (4 samples/lung). According to microcomputed tomography measures, fHP cores were clustered into mild, moderate, and severe fibrosis groups. Gene expression profiles were assessed using weighted gene co-expression network analysis, xCell, gene ontology, and structure enrichment analysis. Gene expression of the prevailing molecular traits was also compared with idiopathic pulmonary fibrosis (IPF). The explant lung findings were evaluated in separate"],"journal":["American journal of respiratory and critical care medicine"],"pubmed_title":["Lung Microenvironments and Disease Progression in Fibrotic Hypersensitivity Pneumonitis."],"pmcid":["PMC8865586"],"funding_grant_id":["W81XWH-19-1-0131","R01HL141852","G065221N","12X9620N","1102020N","1832512N","R21 LM012884","U01 HL145567","R21LM012884","UL1 TR001863","C16/09/005","11V9417N","U01HL145567","UH2 HL123886","1S73921N","R01 HL127349","C24/15/030","R01HL127349","R01 HL141852","UH2HL123886"],"pubmed_authors":["Verleden SE","Geudens V","Martens DS","McDonough JE","Hackett TL","Claes S","Everaerts S","Goos T","Verschakelen JA","Verbeken EK","Decottignies A","Kaminski N","Wuyts WA","Van Herck A","Aelbrecht C","Nawrot TS","Sacreas A","Schupp JC","Yan X","Ackermann M","Vanaudenaerde BM","Vanstapel A","De Sadeleer LJ","Schols D","Mahieu M","Hogg JC"],"additional_accession":[]},"is_claimable":false,"name":"Lung Microenvironments and Disease Progression in Fibrotic Hypersensitivity Pneumonitis.","description":"<b>Rationale:</b> Fibrotic hypersensitivity pneumonitis (fHP) is an interstitial lung disease caused by sensitization to an inhaled allergen. <b>Objectives:</b> To identify the molecular determinants associated with progression of fibrosis. <b>Methods:</b> Nine fHP explant lungs and six unused donor lungs (as controls) were systematically sampled (4 samples/lung). According to microcomputed tomography measures, fHP cores were clustered into mild, moderate, and severe fibrosis groups. Gene expression profiles were assessed using weighted gene co-expression network analysis, xCell, gene ontology, and structure enrichment analysis. Gene expression of the prevailing molecular traits was also compared with idiopathic pulmonary fibrosis (IPF). The explant lung findings were evaluated in separate","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2025-04-22T10:10:44.382Z","creation":"2025-04-05T23:27:12.426Z"},"accession":"S-EPMC8865586","cross_references":{"pubmed":["34724391"],"doi":["10.1164/rccm.202103-0569OC","10.1164/rccm.202103-0569oc"]}}