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Mucosal Associated Invariant T cells in the Obese-asthma endotype

Organization CINCINNATI CHILDRENS HOSP MED CTRLocation CINCINNATI, UNITED STATESPosted 23 Jan 2023Deadline 22 Jan 2026 ⚠️
NIHUS FederalResearch GrantFY20250-11 years old21+ years oldAdipose tissueAdoptive TransferAdultAdult HumanAffectAge of OnsetAllergensAntigen PresentationAsthmaAutomobile DrivingAutoregulationBlood EosinophilBlood NeutrophilBlood Polymorphonuclear NeutrophilBody TissuesBronchial AsthmaC57BL/6 MouseCTLA-8CTLA-8 GeneCTLA8CTLA8 GeneCell BodyCell Communication and SignalingCell SignalingCellsCellular biologyCessation of lifeChildChild YouthChildren (0-21)ChronicClinicalCytotoxic T-Lymphocyte-Associated Antigen 8Cytotoxic T-Lymphocyte-Associated Antigen 8 GeneCytotoxic T-Lymphocyte-Associated Serine Esterase 8Cytotoxic T-Lymphocyte-Associated Serine Esterase 8 GeneDataDeathDevelopmentDiseaseDisorderDisproportionate number of femalesDisproportionate number of womenDisproportionately affects femalesDisproportionately affects womenDisproportionately impacts femalesDisproportionately impacts womenDisproportionately in femalesDisproportionately in womenDysfunctionEosinophilic GranulocyteEosinophilic LeukocyteExperimental ModelsFatty TissueFemaleFrequenciesFunctional disorderGene Expression MonitoringGene Expression Pattern AnalysisGene Expression ProfilingGenetic ModelsHeterogeneityHigh Fat DietHomeostasisHospital AdmissionHospitalizationHouse miceHumanIL-17IL-17 GeneIL-17AIL-17A GeneIL17IL17 ProteinIL17 geneIL17AIL17A GeneImmune responseImmunologyInflammationInflammation MediatorsInflammatoryInterleukin 17 (Cytotoxic T-Lymphocyte-Associated Serine Esterase 8)Interleukin 17 (Cytotoxic T-Lymphocyte-Associated Serine Esterase 8) GeneInterleukin 17 PrecursorInterleukin 17 Precursor GeneInterleukin-17Intermediary MetabolismIntracellular Communication and SignalingKnowledgeLeannessLicensingLigandsLiverLungLung InflammationLung Respiratory SystemMarrow EosinophilMarrow NeutrophilMetabolicMetabolic ProcessesMetabolic dysfunctionMetabolismMiceMice MammalsModalityModelingModern ManMorbid ObesityMorbidityMorbidity - disease rateMucosaMucosal TissueMucous MembraneMurineMusMus musculusNeutrophilic GranulocyteNeutrophilic LeukocyteObesityOutcomePathogenicityPathologicPathologyPatternPersonsPhenotypePhysiological HomeostasisPhysiopathologyPlayPneumonitisPolymorphonuclear CellPolymorphonuclear LeukocytesPolymorphonuclear NeutrophilsPopulationProductionPublic HealthPulmonary InflammationResearchRiskRoleSevere obesitySeveritiesSignal TransductionSignal Transduction SystemsSignalingSymptomsT-CellsT-LymphocyteTemperatureTestingTherapeuticThinnessTimeTissuesTranscript Expression AnalysesTranscript Expression AnalysisWeight GainWeight Increaseadiposeadiposityadulthoodanalyze gene expressionasthma attackasthma exacerbationasthma modelasthmaticbiological sexbiological signal transductionbody weight gainbody weight increasebowel inflammationcell biologycell typecorpulencecytokinedesigndesigningdevelopmentaldiet controldietary controldisease modeldisorder modeldrivingeosinophilexacerbation in asthmaexacerbation prone asthmaexacerbation prone asthmaticextreme obesityfeedingfemale biasfemale outcomesfemale predominancefemale preponderancegene expression analysisgene expression assaygene manipulationgenetic manipulationgenetically manipulategenetically perturbgut inflammationhepatic body systemhepatic organ systemhigh standardhost responsehuman diseasehuman modelimmune system responseimmunoresponseimprovedinflamed bowelinflamed gutinflamed intestineinflammatory lung diseaseinflammatory mediatorinnovateinnovationinnovativeintestinal inflammationkidslung developmentlung functionmalemigrationmodel of humanmortalitymouse modelmurine modelneutrophilnovelobese asthmaobesity-associated asthmaobesity-related asthmaoutcomes among femalesoutcomes among womenoutcomes in femalesoutcomes in womenpathophysiologypoor health outcomepredominance in femalespredominance in womenprotective effectpulmonary functionrecruitreduced health outcomeresistance to therapyresistant to therapysocial roletherapeutic resistancetherapy resistantthymus derived lymphocytetranscriptional profilingtreatment resistancewhite adipose tissuewomen's outcomeswomen's predominancewomen's preponderanceworse health outcomewt gainyellow adipose tissueyoungster

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ABSTRACT
Asthma is an inflammatory lung disease that affects >300 million people worldwide. Although mild asthma is

driven by a Th2-associated, eosinophil-dominated immune response, factors such as obesity/metabolic

dysfunction are associated with more severe asthma. Thus, the “obese asthma” endotype is associated with

frequent asthma…

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Mucosal Associated Invariant T cells in the Obese-asthma endotype — CINCINNATI CHILDRENS HOSP MED CTR | UNITED STATES | | Dev Procure