grant

Mechanisms driving airway inflammation in chronic lung disease

Organization VETERANS HEALTH ADMINISTRATIONLocation ANN ARBOR, UNITED STATESPosted 1 Apr 2014Deadline 30 Jun 2028
VANIHUS FederalResearch GrantFY202519S Gamma GlobulinAdaptive Immune SystemAdoptive TransferAirway ResistanceAntibiotic AgentsAntibiotic DrugsAntibioticsAntigen PresentationAutomobile DrivingBacteriaBlood NeutrophilBlood Polymorphonuclear NeutrophilBlood monocyteCD4 CellsCD4 Positive T LymphocytesCD4 T cellsCD4 helper T cellCD4 lymphocyteCD4+ T-LymphocyteCD4-Positive LymphocytesCOPDCTLA-8CTLA-8 GeneCTLA8CTLA8 GeneCell BodyCell Communication and SignalingCell SignalingCellsChronic Obstruction Pulmonary DiseaseChronic Obstructive Lung DiseaseChronic Obstructive Pulmonary DiseaseChronic lung diseaseCytotoxic T-Lymphocyte-Associated Antigen 8Cytotoxic T-Lymphocyte-Associated Antigen 8 GeneCytotoxic T-Lymphocyte-Associated Serine Esterase 8Cytotoxic T-Lymphocyte-Associated Serine Esterase 8 GeneDataDefectDendritic CellsDevelopmentDiseaseDisease ProgressionDisorderDown-RegulationEctopic lymphoid organEctopic lymphoid structureElderlyEmphysemaEpithelial CellsEpitheliumExocrine IgAExposure toFundingGenerationsGranulocyte ElastaseHost DefenseHumanIL-17IL-17 GeneIL-17AIL-17A GeneIL17IL17 ProteinIL17 geneIL17AIL17A GeneIgAIgMImmuneImmune Cell ActivationImmune GlobulinsImmunesImmunityImmunoglobulin AImmunoglobulin MImmunoglobulinsImpairmentIndividualInflammationInflammatoryInnate Immune SystemInnate ImmunityInterleukin 17 (Cytotoxic T-Lymphocyte-Associated Serine Esterase 8)Interleukin 17 (Cytotoxic T-Lymphocyte-Associated Serine Esterase 8) GeneInterleukin 17 PrecursorInterleukin 17 Precursor GeneInterleukin-17InterventionIntracellular Communication and SignalingInvadedKnowledgeLeukocyte ElastaseLinkLungLung Respiratory SystemLymphatic cellLymphocyteLymphocyte DepletionLymphocyticLysosomal ElastaseMarrow NeutrophilMarrow monocyteMediatingMiceMice MammalsMiscellaneous AntibioticModelingModern ManMucosaMucosal ImmunityMucosal TissueMucous MembraneMurineMusNative ImmunityNatural ImmunityNeutrophil ElastaseNeutrophilic GranulocyteNeutrophilic LeukocyteNon-Specific ImmunityNonspecific ImmunityOralPMN ElastasePathogenicityPathologicPathologyPathway interactionsPatientsPoly-Ig ReceptorPolyimmunoglobulin ReceptorPolymeric Ig ReceptorPolymeric Immunoglobulin ReceptorsPolymorphonuclear CellPolymorphonuclear Leukocyte ElastasePolymorphonuclear LeukocytesPolymorphonuclear NeutrophilsPopulationProductionPulmonary EmphysemaPulmonary PathologyRespiratory EpitheliumRoleSIgASecretory IgASecretory Immunoglobulin ASignal TransductionSignal Transduction SystemsSignalingStructureStructure of respiratory epitheliumSurfaceT-Cell DepletionT-CellsT-LymphocyteT-cell depletion therapyT-lymphocyte depletion therapyT4 CellsT4 LymphocytesTertiary lymphoid structureTestingVeiled CellsVeteransWorkacquired immune systemadaptive immunityadvanced ageairway epitheliumairway epithelium inflammationairway inflammationairway remodelingbiological signal transductioncease smokingchronic obstructive pulmonary disorderchronic pulmonary diseasecigarette smoke exposurecytokinedevelopmentaldimerdisease modeldisorder modeldrivingemphysematousend stage diseaseexperimentexperimental researchexperimental studyexperimentsexposure to cigarette smokegeriatricgerm free conditionhypoimmunityimmune activationimmune deficiencyimmunodeficiencyinjury to tissuelung pathologylymph celllymphocyte depletion therapymonocyteneutrophilnovelpathwayquit smokingreceptor expressionrecruitrespiratory inflammationrespiratory tract epitheliumrespiratory tract inflammationsenior citizensmoking cessationsocial rolespecific pathogen freestop smokingsynergismtertiary lymphoid organthymus derived lymphocytetissue injuryupstream kinase
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Description preview

In the current funding period, we showed that acquired defects in mucosal immunity in small airways are a
central feature of chronic obstructive pulmonary disease (COPD). We now propose to investigate mechanisms

by which impairment of this first line of host defense leads to persistent activation of subsequent lines of host

defense (innate and…

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Mechanisms driving airway inflammation in chronic lung disease — VETERANS HEALTH ADMINISTRATION | UNITED STATES | Apr 20 | Dev Procure