grant
Bacterial lipases and adaptation to the host lipid environment
Organization UNIVERSITY OF ILLINOIS AT CHICAGOLocation Chicago, UNITED STATESPosted 1 Feb 2026Deadline 31 Jan 2031
NIHUS FederalResearch GrantFY2026Animal ModelAnimal Models and Related StudiesAssayAutoregulationBacteremiaBacterial InfectionsBioassayBiochemicalBiogenesisBiological AssayBlocking AntibodiesBlood CirculationBloodstreamBody TissuesBody Weight decreasedCalibrationCardiovascular DiseasesCell BodyCell Communication and SignalingCell SignalingCellsCellulitisDataDevelopmentDiseaseDisorderDisparateDrug Metabolic DetoxicationDrug Metabolic DetoxificationEndocarditisEnvironmentEnzyme GeneEnzymesEsterificationEstersFatty AcidsGram-Positive BacteriaGrantHeartHomeostasisHydrolysisImmuneImmune EvasionImmunesImmunityImmunochemical ImmunologicImmunologicImmunologicalImmunologicallyImmunologicsImmunomodulationInfectionInfection ControlInfectious AgentInfectious Skin DiseasesInflammationInflammatoryInnate Immune ResponseInnate ImmunityIntracellular Communication and SignalingInvestigationKO miceKidneyKidney Urinary SystemKnock-out MiceKnockout MiceKnowledgeLDLLDL LipoproteinsLecithinasesLinkLipaseLipidsLipoprotein (a)Lipoprotein Lp(a)LipoproteinsLiverLow-Density LipoproteinsLp(a)LungLung Respiratory SystemLung SurfactantMacrophageMammalian CellMediatingMembraneMetabolic Drug DetoxicationsMetabolism of Toxic AgentsModelingMolecularMφNative ImmunityNatural ImmunityNon-Specific ImmunityNonspecific ImmunityNull MouseNutrientOrigin of LifeOxidative BurstPathogenesisPatternPenetrationPhosphatidesPhospholipasePhospholipidsPhysiological HomeostasisPhysiologyPneumoniaProductionPropertyPulmonary SurfactantsResearchRespiratory BurstRoleS aureusS. aureusS. aureus infectionSepsisSignal InductionSignal TransductionSignal Transduction SystemsSignalingSiteSkinSpleenSpleen Reticuloendothelial SystemStaph aureusStaph aureus infectionStaphylococcus aureusStaphylococcus aureus infectionSystemic infectionTIL4TLR proteinTLR2TLR2 geneTLR2 receptorTestingTissuesToll-Like Receptor 2Toll-Like Receptor Family GeneToll-like receptorsToll/Interleukin 1 Receptor-Like 4Toll/Interleukin 1 Receptor-Like 4 GeneToll/Interleukin 1 Receptor-Like Protein 4Triacylglycerol HydrolaseTriacylglycerol LipaseTriacylglycerol acylhydrolaseTributyrinaseTriglyceridaseTriglyceride LipaseTriolean HydrolaseUnsaturated Fatty AcidsVirulenceWeight LossWeight ReductionWorkanti-microbialantimicrobialbacteraemiabacteria infectionbacteria pathogenbacterial bloodstream infectionbacterial diseasebacterial infection in the bloodstreambacterial pathogenbeta-Lipoproteinsbiological signal transductionbody weight lossbranched chain fatty acidcardiovascular disordercutaneous infectioncutaneous lesionscytokinedermal lesiondetoxificationdevelopmentalfat metabolismfitnesshepatic body systemhepatic organ systemhost microbe associationhost microbe relationshiphost-microbe interactionshost-microbial interactionshost-microorganism interactionsimmune evasiveimmune modulationimmune regulationimmunologic reactivity controlimmunomodulatoryimmunoregulationimmunoregulatoryinfected skininfected with S. aureusinfected with Staph aureusinfected with Staphylococcus aureusinfectious organisminterestleukocyte oxidative burstlipid metabolismmembrane structuremodel of animalmutantparticlepathogenpathogenic bacteriaprotein purificationrecruitrenalresponseskin infectionskin lesionsocial roletributyraseuptakewt-loss
Description preview
Project Summary
The host lipid environment is a well-described barrier to bacterial infection at several sites including the skin,
lung, and upper airways. In addition, both bacterial and host lipids serve as signals that promote inflammation.
Bacterial lipids activate Toll-like receptors which initiates cytokine production, immune cell…
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