2024
Context‐specific anti‐inflammatory roles of type III interferon signaling in the lung in nonviral injuries
Feng J, Kim J, Wang V, Chang D, Liu H, Bain W, Robinson K, Jie Z, Kotenko S, Dela Cruz C, Sharma L. Context‐specific anti‐inflammatory roles of type III interferon signaling in the lung in nonviral injuries. Physiological Reports 2024, 12: e70104. PMID: 39455422, PMCID: PMC11511623, DOI: 10.14814/phy2.70104.Peer-Reviewed Original ResearchConceptsIII interferon signalingType III interferon signalingLung injuryInterferon signalingBleomycin-induced weight lossInflammatory responseModel of lung injuryBacterial pathogen Pseudomonas aeruginosaAcute lung injuryPathogen Pseudomonas aeruginosaBacterial endotoxin LPSChemotherapeutic agent bleomycinType III interferonsAnti-inflammatory roleIncreased inflammatory signalingLate time pointsBleomycin modelKnockout miceEndotoxin LPSIII interferonsAntiviral cytokinesDay 3Inflammatory signalingEarly injuryImpaired recovery
2022
Epidermal Growth Factor Receptor Inhibition Is Protective in Hyperoxia‐Induced Lung Injury
Harris ZM, Sun Y, Joerns J, Clark B, Hu B, Korde A, Sharma L, Shin HJ, Manning EP, Placek L, Unutmaz D, Stanley G, Chun H, Sauler M, Rajagopalan G, Zhang X, Kang MJ, Koff JL. Epidermal Growth Factor Receptor Inhibition Is Protective in Hyperoxia‐Induced Lung Injury. Oxidative Medicine And Cellular Longevity 2022, 2022: 9518592. PMID: 36193076, PMCID: PMC9526641, DOI: 10.1155/2022/9518592.Peer-Reviewed Original ResearchConceptsAcute lung injuryEpidermal growth factor receptorAlveolar epithelial cellsLung injurySevere hyperoxiaEGFR inhibitionEpithelial cellsHyperoxia-Induced Lung InjuryRole of EGFRMurine alveolar epithelial cellsGrowth factor receptor inhibitionWorse clinical outcomesEpidermal growth factor receptor inhibitionHuman alveolar epithelial cellsWild-type littermatesPoly (ADP-ribose) polymeraseTerminal dUTP nickGrowth factor receptorClinical outcomesImproved survivalReceptor inhibitionLung repairProtective roleComplex roleEGFR deletion
2021
RIPK3 Activates MLKL-mediated Necroptosis and Inflammasome Signaling during Streptococcus Infection.
Huang HR, Cho SJ, Harris RM, Yang J, Bermejo S, Sharma L, Dela Cruz CS, Xu JF, Stout-Delgado HW. RIPK3 Activates MLKL-mediated Necroptosis and Inflammasome Signaling during Streptococcus Infection. American Journal Of Respiratory Cell And Molecular Biology 2021, 64: 579-591. PMID: 33625952, PMCID: PMC8086037, DOI: 10.1165/rcmb.2020-0312oc.Peer-Reviewed Original ResearchMeSH KeywordsAgedAnimalsCalcium ChannelsCase-Control StudiesDisease Models, AnimalFemaleGene Expression RegulationHumansInflammasomesMacrophages, AlveolarMaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedMitochondriaMitochondrial Permeability Transition PoreNecroptosisNLR Family, Pyrin Domain-Containing 3 ProteinPneumonia, PneumococcalProtein KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesReceptor-Interacting Protein Serine-Threonine KinasesSignal TransductionStreptococcus pneumoniaeConceptsCommunity-acquired pneumoniaPneumococcal pneumoniaSevere pathological damageHealthy control subjectsPotential plasma markerNLRP3 inflammasome activationCommon bacterial pathogensMitochondrial permeability transition pore openingStreptococcal pneumoniaPlasma markersStreptococcus infectionBacterial clearanceControl subjectsPathological damageLeading causeMitochondrial reactive oxygenInflammasome activationMurine modelMitochondrial calcium uptakePneumoniaPermeability transition pore openingHuman studiesHigh mortalityInflammasome signalingTransition pore opening
2020
Severe respiratory viral infection induces procalcitonin in the absence of bacterial pneumonia
Gautam S, Cohen AJ, Stahl Y, Toro P, Young GM, Datta R, Yan X, Ristic NT, Bermejo SD, Sharma L, Restrepo M, Dela Cruz CS. Severe respiratory viral infection induces procalcitonin in the absence of bacterial pneumonia. Thorax 2020, 75: 974-981. PMID: 32826284, DOI: 10.1136/thoraxjnl-2020-214896.Peer-Reviewed Original ResearchConceptsPure viral infectionBacterial coinfectionViral infectionInfluenza infectionSevere respiratory viral infectionsAbility of procalcitoninRetrospective cohort studyViral respiratory infectionsRespiratory viral infectionsMarker of severityRespiratory viral illnessSevere viral infectionsSpecificity of procalcitoninCharacteristic curve analysisCellular modelHigher procalcitoninProcalcitonin expressionElevated procalcitoninCohort studyViral illnessRespiratory infectionsAntibiotic administrationBacterial pneumoniaSevere diseaseProcalcitonin
2019
A potential role of microvesicle-containing miR-223/142 in lung inflammation
Zhang D, Lee H, Wang X, Groot M, Sharma L, Dela Cruz CS, Jin Y. A potential role of microvesicle-containing miR-223/142 in lung inflammation. Thorax 2019, 74: 865-874. PMID: 31331947, PMCID: PMC7036165, DOI: 10.1136/thoraxjnl-2018-212994.Peer-Reviewed Original ResearchConceptsAcute lung injuryNLRP3 inflammasome activationLung inflammationInflammasome activationMacrophage-mediated inflammatory responsesBronchoalveolar lavage fluid samplesIntratracheal lipopolysaccharide (LPS) instillationUncontrolled lung inflammationInhibition of NLRP3Inflammatory lung responseLavage fluid samplesFunctions of microvesiclesLung injuryLipopolysaccharide instillationLung responseIntratracheal instillationInflammatory responseLung macrophagesMurine lungMacrophage activationMiR-223BALFInflammationLPSMiR-142
2018
Impact of Cigarette Smoke Exposure on the Lung Fibroblastic Response after Influenza Pneumonia
Lee SW, Sharma L, Kang YA, Kim SH, Chandrasekharan S, Losier A, Brady V, Bermejo S, Andrews N, Yoon CM, Liu W, Lee JY, Kang MJ, Dela Cruz CS. Impact of Cigarette Smoke Exposure on the Lung Fibroblastic Response after Influenza Pneumonia. American Journal Of Respiratory Cell And Molecular Biology 2018, 59: 770-781. PMID: 30110182, PMCID: PMC6293077, DOI: 10.1165/rcmb.2018-0004oc.Peer-Reviewed Original ResearchConceptsCigarette smoke exposureLungs of miceInfluenza infectionInfluenza virusBAL fluidSmoke exposureGrowth factor-β1 levelsAir-exposed lungsInfluenza-infected miceSignificant lung injuryFibroblastic responseLung-derived fibroblastsProtein-positive cellsGrowth factor-β1Influenza pneumoniaDifferent time pointsLung injurySmoking groupSignificant morbidityCS exposureMurine modelFibrotic responseΒ1 levelsFactor-β1Weight recoveryBPIFA1 regulates lung neutrophil recruitment and interferon signaling during acute inflammation
Britto CJ, Niu N, Khanal S, Huleihel L, Herazo-Maya J, Thompson A, Sauler M, Slade MD, Sharma L, Dela Cruz CS, Kaminski N, Cohn LE. BPIFA1 regulates lung neutrophil recruitment and interferon signaling during acute inflammation. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2018, 316: l321-l333. PMID: 30461288, PMCID: PMC6397348, DOI: 10.1152/ajplung.00056.2018.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsGlycoproteinsInflammationLipopolysaccharidesLungMice, Inbred C57BLNeutrophil InfiltrationPhosphoproteinsConceptsLung inflammationAcute inflammationC motif chemokine ligand 10Lung neutrophil recruitmentRegulation of CXCL10Acute lung inflammationBronchoalveolar lavage concentrationsChemokine ligand 10Innate immune responseIFN regulatory factorIntranasal LPSLavage concentrationsLung recruitmentNeutrophil recruitmentWT miceImmune effectsLung diseasePMN recruitmentInflammatory responseLPS treatmentLung tissueInflammatory signalsImmune responseImmunomodulatory propertiesInflammationThe fungal ligand chitin directly binds TLR2 and triggers inflammation dependent on oligomer size
Fuchs K, Cardona Gloria Y, Wolz O, Herster F, Sharma L, Dillen CA, Täumer C, Dickhöfer S, Bittner Z, Dang T, Singh A, Haischer D, Schlöffel MA, Koymans KJ, Sanmuganantham T, Krach M, Roger T, Le Roy D, Schilling NA, Frauhammer F, Miller LS, Nürnberger T, LeibundGut‐Landmann S, Gust AA, Macek B, Frank M, Gouttefangeas C, Dela Cruz CS, Hartl D, Weber AN. The fungal ligand chitin directly binds TLR2 and triggers inflammation dependent on oligomer size. EMBO Reports 2018, 19: embr201846065. PMID: 30337494, PMCID: PMC6280652, DOI: 10.15252/embr.201846065.Peer-Reviewed Original ResearchConceptsTLR2 ligandsInnate immune receptors Toll-like receptorToll-like receptorsMurine immune cellsImmune activationDistinct signaling outcomesImmune cellsNovel therapiesTriggers inflammationImmuno-modulationFungal infectionsInflammationImmune receptorsPotential targetTLR2Unknown purityReceptorsNanomolar affinityAsthmaHumansTherapyInfectionFungal diseasesDiseasePathology
2016
IL-13Rα2 uses TMEM219 in chitinase 3-like-1-induced signalling and effector responses
Lee CM, He CH, Nour AM, Zhou Y, Ma B, Park JW, Kim KH, Cruz CD, Sharma L, Nasr ML, Modis Y, Lee CG, Elias JA. IL-13Rα2 uses TMEM219 in chitinase 3-like-1-induced signalling and effector responses. Nature Communications 2016, 7: 12752. PMID: 27629921, PMCID: PMC5027616, DOI: 10.1038/ncomms12752.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisCell Line, TumorChitinase-3-Like Protein 1Heparin-binding EGF-like Growth FactorHumansInterleukin-13 Receptor alpha2 SubunitLung InjuryLung NeoplasmsMAP Kinase Signaling SystemMelanoma, ExperimentalMembrane ProteinsMice, Inbred C57BLNeoplasm MetastasisProto-Oncogene Proteins c-aktTransforming Growth Factor beta1Two-Hybrid System TechniquesWnt Signaling PathwayConceptsNull mutationPKB/Akt activationBimolecular fluorescence complementationDirect physical interactionMAPK/ERKHB-EGF productionFluorescence complementationTwo-hybridMembrane proteinsAkt activationDecoy functionPhysical interactionIL-13Rα2Effect of CHI3L1Chitinase 3Critical roleSignalingMutationsRecent studiesCHI3L1ComplementationTGF-β1YeastMelanoma metastasesERK