2016
Uricase Inhibits Nitrogen Dioxide–Promoted Allergic Sensitization to Inhaled Ovalbumin Independent of Uric Acid Catabolism
Ather JL, Burgess EJ, Hoyt LR, Randall MJ, Mandal MK, Matthews DE, Boyson JE, Poynter ME. Uricase Inhibits Nitrogen Dioxide–Promoted Allergic Sensitization to Inhaled Ovalbumin Independent of Uric Acid Catabolism. The Journal Of Immunology 2016, 197: 1720-1732. PMID: 27465529, PMCID: PMC4992621, DOI: 10.4049/jimmunol.1600336.Peer-Reviewed Original ResearchConceptsAllergic airway diseaseAllergic sensitizationAirway diseaseUric acidDevelopment of OVAOVA-specific responsesAirways of miceUric acid levelsAdaptive immune responsesOVA-specific AbT cell proliferationPowerful inhibitory effectEnvironmental air pollutantsImmune deviationOVA challengeOVA uptakeDendritic cellsCytokine productionAdjuvant activityImmune responseRespiratory diseaseMouse modelUric acid formationInhibitory effectAcid levelsWeight Loss Decreases Inherent and Allergic Methacholine Hyperresponsiveness in Mouse Models of Diet-Induced Obese Asthma
Ather JL, Chung M, Hoyt LR, Randall MJ, Georgsdottir A, Daphtary NA, Aliyeva MI, Suratt BT, Bates JH, Irvin CG, Russell SR, Forgione PM, Dixon AE, Poynter ME. Weight Loss Decreases Inherent and Allergic Methacholine Hyperresponsiveness in Mouse Models of Diet-Induced Obese Asthma. American Journal Of Respiratory Cell And Molecular Biology 2016, 55: 176-187. PMID: 27064658, PMCID: PMC4979374, DOI: 10.1165/rcmb.2016-0070oc.Peer-Reviewed Original ResearchConceptsDiet-induced weight lossObese asthmaMethacholine hyperresponsivenessWeight lossAsthma phenotypesMouse modelBariatric surgery-induced weight lossSurgery-induced weight lossFirmicutes/Bacteroidetes ratioAllergic asthma phenotypeDietary weight lossObese-asthma phenotypeSurgical weight lossSuccessful weight lossElevated proinflammatory cytokinesCentral airway resistanceDiet-induced obesityEnvironmental allergen exposureAdaptive immune responsesSubstantial weight lossDistinct anatomical compartmentsMethacholine responsivenessAllergic asthmaAllergen exposureAsthma symptoms
2013
The Endogenous Th17 Response in NO2-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer
Martin RA, Ather JL, Daggett R, Hoyt L, Alcorn JF, Suratt BT, Weiss DJ, Lundblad LK, Poynter ME. The Endogenous Th17 Response in NO2-Promoted Allergic Airway Disease Is Dispensable for Airway Hyperresponsiveness and Distinct from Th17 Adoptive Transfer. PLOS ONE 2013, 8: e74730. PMID: 24069338, PMCID: PMC3778003, DOI: 10.1371/journal.pone.0074730.Peer-Reviewed Original ResearchConceptsAllergic airway diseaseAirway hyperresponsivenessAirway diseaseAdoptive transferAntigen challengeCytokine productionNeutrophil recruitmentIL-1RDevelopment of AHRIL-1 receptor signalingLung cellsGlucocorticoid-resistant asthmaIL-17A neutralizationOTII T cellsAdaptive immune responsesDecreased neutrophil recruitmentAHR developmentClinical asthmaMixed Th2Antigen restimulationSevere asthmaTh17 cellsIL-17Th17 responsesAsthma severity