{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wiesner DL"],"funding":["NCATS NIH HHS","NIAID NIH HHS","Council on Ocean Affairs Science and Technology, California State University","National Heart, Lung, and Blood Institute","NHLBI NIH HHS","National Institutes of Health","Hartwell Foundation","NIDDK NIH HHS","Cystic Fibrosis Foundation","Charles H. Hood Foundation","NCI NIH HHS","North Carolina Biotechnology Center","NIH HHS","NIGMS NIH HHS","National Science Foundation"],"pagination":["614-628.e6"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7305569"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["27(4)"],"pubmed_abstract":["Airway epithelium is the first body surface to contact inhaled irritants and report danger. Here, we report how epithelial cells recognize and respond to aeroallergen alkaline protease 1 (Alp1) of Aspergillus sp., because proteases are critical components of many allergens that provoke asthma. In a murine model, Alp1 elicits helper T (Th) cell-dependent lung eosinophilia that is initiated by the rapid response of bronchiolar club cells to Alp1. Alp1 damages bronchiolar cell junctions, which triggers a calcium flux signaled through calcineurin within club cells of the bronchioles, inciting inflammation. In two human cohorts, we link fungal sensitization and/or asthma with SNP/protein expression of the mechanosensitive calcium channel, TRPV4. TRPV4 is also necessary and sufficient for club c"],"journal":["Cell host & microbe"],"pubmed_title":["Club Cell TRPV4 Serves as a Damage Sensor Driving Lung Allergic Inflammation."],"pmcid":["PMC7305569"],"funding_grant_id":["R37 AI035681","R01 AI136529","UL1 TR002373","T32 HL007899","T32 AI055397","S10 OD018202","P50 GM64598","P30 CA014520","PO1 HL70381","T32 AI007635","T32 GM008692","P01 HL070831","DBI-9977525","R01AI136529","T32 HL116275","1S100OD018202-01","T32 HL07899","R01 AI130411","R01 AI040996","DBI-0520825","UL1 TR000427","R33 DK070297","MOU19G0","R01 AI035681","P50 GM064598"],"pubmed_authors":["Ober C","Brockman-Schneider RA","Freeman M","Klein BS","Keller NP","Mou H","Gern JE","Esnault SJ","Wiesner DL","Warner T","Jackson DJ","Jarjour NN","Vyas JM","Merkhofer RM","Niu M","Evans MD","Feldman MB","Kujoth GC"],"additional_accession":[]},"is_claimable":false,"name":"Club Cell TRPV4 Serves as a Damage Sensor Driving Lung Allergic Inflammation.","description":"Airway epithelium is the first body surface to contact inhaled irritants and report danger. Here, we report how epithelial cells recognize and respond to aeroallergen alkaline protease 1 (Alp1) of Aspergillus sp., because proteases are critical components of many allergens that provoke asthma. In a murine model, Alp1 elicits helper T (Th) cell-dependent lung eosinophilia that is initiated by the rapid response of bronchiolar club cells to Alp1. Alp1 damages bronchiolar cell junctions, which triggers a calcium flux signaled through calcineurin within club cells of the bronchioles, inciting inflammation. In two human cohorts, we link fungal sensitization and/or asthma with SNP/protein expression of the mechanosensitive calcium channel, TRPV4. TRPV4 is also necessary and sufficient for club c","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Apr","modification":"2026-05-01T16:30:54.482Z","creation":"2022-02-09T12:51:57.315Z"},"accession":"S-EPMC7305569","cross_references":{"pubmed":["32130954"],"doi":["10.1016/j.chom.2020.02.006"]}}