2025
cGAS Expression is enhanced in systemic sclerosis associated interstitial lung disease and stimulates inflammatory myofibroblast activation.
Yu S, Hu B, Sun Y, Peng X, Lee C, Woo S, McGovern J, Zielonka J, Saber T, Ghincea A, Gandhi S, Walia A, Pivarnik T, Ishikawa G, Shao S, Sun H, Gunes B, Kujawski S, Perez S, Odell W, Hinchcliff M, Varga J, Feghali-Bostwick C, Sauler M, Gomez J, Ryu C, Herzog E. cGAS Expression is enhanced in systemic sclerosis associated interstitial lung disease and stimulates inflammatory myofibroblast activation. European Respiratory Journal 2025, 2401564. PMID: 40374521, DOI: 10.1183/13993003.01564-2024.Peer-Reviewed Original ResearchPrecision cut lung slicesSSc-ILD lung tissuesType 1 interferonSSc-ILDProduction of cytokinesBronchoalveolar lavageHuman precision cut lung slicesLung tissueLung fibroblastsLungs of patientsInterstitial lung diseasePulmonary fibrosis modelBleomycin mouse modelIsolated lung fibroblastsCultured fibroblastsPerturbs innate immunityFibrotic stimuliSingle cell RNA sequencing datasetsSystemic sclerosisHuman lung fibroblastsLung diseaseMouse modelCyclic GMP-AMP synthaseFibrosis modelTherapeutic approachesT cells of patients with systemic sclerosis or Sjögren’s disease display an aberrant metabolic state and memory phenotype in blood and lungs
Ehlers C, Biermann H, Thiele T, Schupp J, Villa M, Jänke C, Risser L, Witte T, Kalinke U, Seeliger B, Graalmann T. T cells of patients with systemic sclerosis or Sjögren’s disease display an aberrant metabolic state and memory phenotype in blood and lungs. Rheumatology 2025, keaf198. PMID: 40244816, DOI: 10.1093/rheumatology/keaf198.Peer-Reviewed Original ResearchInterstitial lung diseaseCD8+ T cellsT cells of patientsBronchoalveolar lavage of patientsSystemic sclerosisBronchoalveolar lavageT cellsSjogren's diseaseHealthy controlsBlood CD8+ T cellsBlood T cells of patientsLevels of HLA-DRIncreased expression of CD25Involvement of T cellsExpression of CD25Increased CD4+T cell responsesT cell receptor engagementLungs of patientsT cell characterizationExpressed increased levelsCell type 2Aberrant metabolic stateExpressed significant levelsSpectral flow cytometry
2024
CCR2+ monocytes are dispensable to resolve acute pulmonary Pseudomonas aeruginosa infections in WT and cystic fibrosis mice
Öz H, Braga C, Gudneppanavar R, Di Pietro C, Huang P, Zhang P, Krause D, Egan M, Murray T, Bruscia E. CCR2+ monocytes are dispensable to resolve acute pulmonary Pseudomonas aeruginosa infections in WT and cystic fibrosis mice. Journal Of Leukocyte Biology 2024, 117: qiae218. PMID: 39365279, PMCID: PMC11953069, DOI: 10.1093/jleuko/qiae218.Peer-Reviewed Original ResearchLung tissue damageCystic fibrosisTissue damageMonocyte recruitmentImmune responsePulmonary Pseudomonas aeruginosa infectionHyper-inflammatory immune responseCystic fibrosis micePropagate tissue damagePseudomonas aeruginosaLungs of patientsChronic neutrophilic inflammationImmunological response to infectionHost immune responseMonocyte-derived macrophagesTarget monocyte recruitmentSite of injuryResponse to infectionCFTR modulatorsPA infectionChronic inflammatory disease conditionsReduced bactericidal activityAdjunctive therapyClinical outcomesEradicate infection
2022
Ameliorating Fibrosis in Murine and Human Tissues with END55, an Endostatin-Derived Fusion Protein Made in Plants
Mlakar L, Garrett S, Watanabe T, Sanderson M, Nishimoto T, Heywood J, Helke K, Pilewski J, Herzog E, Feghali-Bostwick C. Ameliorating Fibrosis in Murine and Human Tissues with END55, an Endostatin-Derived Fusion Protein Made in Plants. Biomedicines 2022, 10: 2861. PMID: 36359382, PMCID: PMC9687961, DOI: 10.3390/biomedicines10112861.Peer-Reviewed Original ResearchAnti-fibrotic effectsIdiopathic pulmonary fibrosisSystemic sclerosisPulmonary fibrosisLung fibrosisMouse modelSignificant anti-fibrotic effectEffective anti-fibrotic therapiesBleomycin mouse modelLungs of patientsAnti-fibrotic therapiesPrevention of skinSecond mouse modelCollagen XVIII/endostatinGrowth factor-β1Matrix-degrading enzymesLung transplantationSignificant morbidityHuman tissuesLung diseaseHealth burdenEffective treatmentFactor-β1Organ fibrosisFibrosis
2020
Comprehensive T cell repertoire characterization of non-small cell lung cancer
Reuben A, Zhang J, Chiou SH, Gittelman RM, Li J, Lee WC, Fujimoto J, Behrens C, Liu X, Wang F, Quek K, Wang C, Kheradmand F, Chen R, Chow CW, Lin H, Bernatchez C, Jalali A, Hu X, Wu CJ, Eterovic AK, Parra ER, Yusko E, Emerson R, Benzeno S, Vignali M, Wu X, Ye Y, Little LD, Gumbs C, Mao X, Song X, Tippen S, Thornton RL, Cascone T, Snyder A, Wargo JA, Herbst R, Swisher S, Kadara H, Moran C, Kalhor N, Zhang J, Scheet P, Vaporciyan AA, Sepesi B, Gibbons DL, Robins H, Hwu P, Heymach JV, Sharma P, Allison JP, Baladandayuthapani V, Lee JJ, Davis MM, Wistuba II, Futreal PA, Zhang J. Comprehensive T cell repertoire characterization of non-small cell lung cancer. Nature Communications 2020, 11: 603. PMID: 32001676, PMCID: PMC6992630, DOI: 10.1038/s41467-019-14273-0.Peer-Reviewed Original ResearchConceptsNon-small cell lung cancerCell lung cancerT cellsLung cancerAdoptive T-cell therapyEarly-stage NSCLC patientsT cell repertoire analysisT cell responsesLungs of patientsT-cell therapyNSCLC patientsInferior survivalClinicopathologic featuresImmune landscapeViral infectionSolid tumorsTherapeutic efficacyCell responsesCell therapyPatientsRepertoire analysisLungTumorsImmunotherapyConsiderable proportion
2014
Chitinase 3–Like 1 Suppresses Injury and Promotes Fibroproliferative Responses in Mammalian Lung Fibrosis
Zhou Y, Peng H, Sun H, Peng X, Tang C, Gan Y, Chen X, Mathur A, Hu B, Slade MD, Montgomery RR, Shaw AC, Homer RJ, White ES, Lee CM, Moore MW, Gulati M, Lee CG, Elias JA, Herzog EL. Chitinase 3–Like 1 Suppresses Injury and Promotes Fibroproliferative Responses in Mammalian Lung Fibrosis. Science Translational Medicine 2014, 6: 240ra76. PMID: 24920662, PMCID: PMC4340473, DOI: 10.1126/scitranslmed.3007096.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisCHI3L1 levelsChitinase 3Lungs of patientsAlternative macrophage activationLevel of apoptosisAcute exacerbationFibroproliferative repairLung transplantationDisease exacerbationInjury phaseAmbulatory patientsEpithelial injuryPulmonary fibrosisIPF populationLung fibrosisMacrophage accumulationCHI3L1 expressionFibrotic phaseDisease progressionProfibrotic roleFibroproliferative responseMacrophage activationMyofibroblast transformationProtective role
2012
Retinoic Acid–related Orphan Receptor-α Is Induced in the Setting of DNA Damage and Promotes Pulmonary Emphysema
Shi Y, Cao J, Gao J, Zheng L, Goodwin A, An CH, Patel A, Lee JS, Duncan SR, Kaminski N, Pandit KV, Rosas IO, Choi AM, Morse D. Retinoic Acid–related Orphan Receptor-α Is Induced in the Setting of DNA Damage and Promotes Pulmonary Emphysema. American Journal Of Respiratory And Critical Care Medicine 2012, 186: 412-419. PMID: 22744720, PMCID: PMC5450975, DOI: 10.1164/rccm.201111-2023oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersCells, CulturedDisease Models, AnimalDNA DamageDNA RepairGene Expression ProfilingHumansLungMiceMice, Inbred C57BLMice, Neurologic MutantsNuclear Receptor Subfamily 1, Group F, Member 1Oligonucleotide Array Sequence AnalysisPulmonary Disease, Chronic ObstructivePulmonary EmphysemaTobacco Smoke PollutionConceptsRetinoic acid-related orphan receptorAcid-related orphan receptorCigarette smoke extractLungs of patientsPathogenesis of emphysemaRORA expressionCigarette smokeAirspace enlargementSmoke extractCigarette smoke exposureSmoke-induced emphysemaOrphan receptorDNA damageActive smokingLung transplantationSmoke exposureLung cancerPulmonary emphysemaLung tissueEmphysemaPatientsGene expression profilingApoptotic cell deathMiceEnhanced susceptibility
2010
miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis
Liu G, Friggeri A, Yang Y, Milosevic J, Ding Q, Thannickal VJ, Kaminski N, Abraham E. miR-21 mediates fibrogenic activation of pulmonary fibroblasts and lung fibrosis. Journal Of Experimental Medicine 2010, 207: 1589-1597. PMID: 20643828, PMCID: PMC2916139, DOI: 10.1084/jem.20100035.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsAntisense Elements (Genetics)BleomycinCell LineCollagenExtracellular Matrix ProteinsFibroblastsFibronectinsGene ExpressionHumansIdiopathic Pulmonary FibrosisLungMiceMice, Inbred C57BLMice, TransgenicMicroRNAsOligonucleotidesPhosphorylationPulmonary FibrosisSmad2 ProteinSmad7 ProteinTransforming Growth Factor beta1ConceptsIdiopathic pulmonary fibrosisFibrotic lung diseaseMiR-21 expressionMiR-21Fibrotic diseasesLung diseaseLung fibrosisPulmonary fibroblastsPrimary pulmonary fibroblastsPro-fibrogenic activityLungs of patientsLungs of miceExperimental lung fibrosisMiR-21 levelsPulmonary injuryInjury contributesPulmonary fibrosisPathological mediatorsPathophysiologic processesDysregulation of miRNAsFibrogenic activationFibrosisDiseaseExtracellular matrix productionFatal process
2009
Decreased Expression of Cholesterol and Fatty Acid Synthesis Genes in Lungs of Patients with Pulmonary Fibrosis.
Geyer A, Gochuico B, Kaminski N, Morse D, Rosas I. Decreased Expression of Cholesterol and Fatty Acid Synthesis Genes in Lungs of Patients with Pulmonary Fibrosis. 2009, a1912. DOI: 10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1912.Peer-Reviewed Original Research
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