2024
Development and evaluation of a questionnaire to capture environmental and occupational inhalational exposures in adults with fibrotic interstitial lung disease
Swaminathan A, McFatrich M, Mkumba L, Wright L, Redlich C, Snyder L, Reeve B, Patel D, Gulati M. Development and evaluation of a questionnaire to capture environmental and occupational inhalational exposures in adults with fibrotic interstitial lung disease. Respiratory Research 2024, 25: 372. PMID: 39407223, PMCID: PMC11481565, DOI: 10.1186/s12931-024-03000-z.Peer-Reviewed Original ResearchConceptsCognitive interviewsContent validityExposure questionnaireMultidisciplinary teamSemi-structured interview guideEvidence of content validityFibrosing ILDsInterstitial lung diseaseRelevant exposuresFibrotic interstitial lung diseaseClinically relevant exposuresTrained interviewersInterview guideAssessment QuestionnaireQuestionnaireInterviewsLung diseaseAdultsTeamClinicPatientsSource of misunderstandingOccupational inhalation exposureValidityDisease
2021
Macrophage-derived netrin-1 drives adrenergic nerve–associated lung fibrosis
Gao R, Peng X, Perry C, Sun H, Ntokou A, Ryu C, Gomez JL, Reeves BC, Walia A, Kaminski N, Neumark N, Ishikawa G, Black KE, Hariri LP, Moore MW, Gulati M, Homer RJ, Greif DM, Eltzschig HK, Herzog EL. Macrophage-derived netrin-1 drives adrenergic nerve–associated lung fibrosis. Journal Of Clinical Investigation 2021, 131: e136542. PMID: 33393489, PMCID: PMC7773383, DOI: 10.1172/jci136542.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBleomycinFemaleLungMacrophagesMaleMiceMice, TransgenicNetrin-1NorepinephrinePulmonary FibrosisConceptsNetrin-1Lung fibrosisCell-specific knockout miceΑ1-adrenoreceptor blockadeIPF lung tissueNeuronal guidance proteinsNetrin-1 expressionExtracellular matrix accumulationAdrenergic processesAdrenoreceptor antagonismAdrenoreceptor blockadeFibrotic histologyInflammatory scarringIPF cohortAdrenergic nervesΑ1-blockersImproved survivalColorectal carcinomaLung tissueKnockout miceCollagen accumulationFibrosisMatrix accumulationMacrophagesGuidance proteins
2020
Diagnosis of Hypersensitivity Pneumonitis in Adults. An Official ATS/JRS/ALAT Clinical Practice Guideline
Raghu G, Remy-Jardin M, Ryerson CJ, Myers JL, Kreuter M, Vasakova M, Bargagli E, Chung JH, Collins BF, Bendstrup E, Chami HA, Chua AT, Corte TJ, Dalphin JC, Danoff SK, Diaz-Mendoza J, Duggal A, Egashira R, Ewing T, Gulati M, Inoue Y, Jenkins AR, Johannson KA, Johkoh T, Tamae-Kakazu M, Kitaichi M, Knight SL, Koschel D, Lederer DJ, Mageto Y, Maier LA, Matiz C, Morell F, Nicholson AG, Patolia S, Pereira CA, Renzoni EA, Salisbury ML, Selman M, Walsh SLF, Wuyts WA, Wilson KC. Diagnosis of Hypersensitivity Pneumonitis in Adults. An Official ATS/JRS/ALAT Clinical Practice Guideline. American Journal Of Respiratory And Critical Care Medicine 2020, 202: e36-e69. PMID: 32706311, PMCID: PMC7397797, DOI: 10.1164/rccm.202005-2032st.Peer-Reviewed Original ResearchConceptsSurgical lung biopsyHypersensitivity pneumonitisLung biopsyGuidelines CommitteeDiagnosis of HPFibrotic hypersensitivity pneumonitisNonfibrotic hypersensitivity pneumonitisTransbronchial lung biopsyTransbronchial lung cryobiopsyInterstitial lung diseaseJapanese Respiratory SocietyBronchoalveolar lavage fluidClinical practice guidelinesAmerican Thoracic SocietyPotential exposureGRADE approachLung cryobiopsyLavage fluidSerum IgGLung diseasePathological featuresThorough historyRespiratory SocietyThoracic SocietyPractice guidelines
2016
Plexin C1 deficiency permits synaptotagmin 7–mediated macrophage migration and enhances mammalian lung fibrosis
Peng X, Moore M, Mathur A, Zhou Y, Sun H, Gan Y, Herazo‐Maya J, Kaminski N, Hu X, Pan H, Ryu C, Osafo‐Addo A, Homer RJ, Feghali‐Bostwick C, Fares W, Gulati M, Hu B, Lee C, Elias JA, Herzog EL. Plexin C1 deficiency permits synaptotagmin 7–mediated macrophage migration and enhances mammalian lung fibrosis. The FASEB Journal 2016, 30: 4056-4070. PMID: 27609773, PMCID: PMC5102121, DOI: 10.1096/fj.201600373r.Peer-Reviewed Original ResearchConceptsLung fibrosisPlexin C1Macrophage migrationPulmonary fibrosisBone marrow-derived cellsSynaptotagmin-7Idiopathic pulmonary fibrosisInterstitial lung diseaseMarrow-derived cellsTGF-β1 overexpressionFatal conditionLung diseaseMonocyte migrationUnrecognized observationCollagen accumulationFibrosisMice showBoyden chamberGenetic deletionLungMouse macrophagesSemaphorin receptorsMacrophagesC1s deficiencyDeficiencyNetrin‐1 Regulates Fibrocyte Accumulation in the Decellularized Fibrotic Sclerodermatous Lung Microenvironment and in Bleomycin‐Induced Pulmonary Fibrosis
Sun H, Zhu Y, Pan H, Chen X, Balestrini JL, Lam TT, Kanyo JE, Eichmann A, Gulati M, Fares WH, Bai H, Feghali-Bostwick CA, Gan Y, Peng X, Moore MW, White ES, Sava P, Gonzalez AL, Cheng Y, Niklason LE, Herzog EL. Netrin‐1 Regulates Fibrocyte Accumulation in the Decellularized Fibrotic Sclerodermatous Lung Microenvironment and in Bleomycin‐Induced Pulmonary Fibrosis. Arthritis & Rheumatology 2016, 68: 1251-1261. PMID: 26749424, PMCID: PMC5547894, DOI: 10.1002/art.39575.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibiotics, AntineoplasticAntibodies, NeutralizingBiomechanical PhenomenaBleomycinCase-Control StudiesCell DifferentiationCollagenCollagen Type ICollagen Type I, alpha 1 ChainFibrosisFlow CytometryFluorescent Antibody TechniqueHeterozygoteHumansLeukocyte Common AntigensLeukocytes, MononuclearLungLung Diseases, InterstitialMiceMice, KnockoutMicroscopy, Electron, ScanningNerve Growth FactorsNetrin-1ProteomicsPulmonary FibrosisReverse Transcriptase Polymerase Chain ReactionScleroderma, SystemicTissue ScaffoldsTumor Suppressor ProteinsConceptsSSc-related interstitial lung diseaseInterstitial lung diseaseFibrocyte accumulationNetrin-1Lung extracellular matrixPulmonary fibrosisLung scaffoldsBleomycin-Induced Pulmonary FibrosisPeripheral blood mononuclear cellsBlood mononuclear cellsHealthy control subjectsNovel therapeutic targetSystemic sclerosisExtracellular matrixLung fibrosisLung diseaseMononuclear cellsControl subjectsLung microenvironmentHealthy controlsScleroderma patientsAberrant anatomyLung matrixPatientsTherapeutic target
2015
Chitinase 3–like–1 and its receptors in Hermansky-Pudlak syndrome–associated lung disease
Zhou Y, He CH, Herzog EL, Peng X, Lee CM, Nguyen TH, Gulati M, Gochuico BR, Gahl WA, Slade ML, Lee CG, Elias JA. Chitinase 3–like–1 and its receptors in Hermansky-Pudlak syndrome–associated lung disease. Journal Of Clinical Investigation 2015, 125: 3178-3192. PMID: 26121745, PMCID: PMC4563747, DOI: 10.1172/jci79792.Peer-Reviewed Original ResearchMeSH KeywordsAdipokinesAdultAnimalsApoptosisBiomarkersChitinase-3-Like Protein 1Disease Models, AnimalFemaleGlycoproteinsHermanski-Pudlak SyndromeHumansInterleukin-13 Receptor alpha2 SubunitLectinsMaleMiceMice, KnockoutPulmonary FibrosisReceptors, ImmunologicReceptors, ProstaglandinRespiratory MucosaConceptsHermansky-Pudlak syndromePulmonary fibrosisChitinase 3Pulmonary fibrosis progressionFibroproliferative repairCHI3L1 levelsFibrosis progressionLung diseaseHPS-4HPS patientsIL-13Rα2Effector functionsReceptor CRTH2Epithelial apoptosisFibrosisProtective roleDisease severityPotential biomarkersCHI3L1Major causeHPS-1Abnormal localizationPatientsCell deathSeverity
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
2011
Role of semaphorin 7a signaling in transforming growth factor β1–induced lung fibrosis and scleroderma‐related interstitial lung disease
Gan Y, Reilkoff R, Peng X, Russell T, Chen Q, Mathai SK, Homer R, Gulati M, Siner J, Elias J, Bucala R, Herzog E. Role of semaphorin 7a signaling in transforming growth factor β1–induced lung fibrosis and scleroderma‐related interstitial lung disease. Arthritis & Rheumatism 2011, 63: 2484-2494. PMID: 21484765, PMCID: PMC3651701, DOI: 10.1002/art.30386.Peer-Reviewed Original ResearchConceptsPeripheral blood mononuclear cellsInterstitial lung diseaseBone marrow-derived cellsMarrow-derived cellsSemaphorin 7AGrowth factor-β1Lung diseaseLung fibrosisFactor-β1Human peripheral blood mononuclear cellsNormal human peripheral blood mononuclear cellsSemaphorin 7a expressionBone marrow transplantationBlood mononuclear cellsReceptor β1 integrinΒ1 integrinFibrocyte differentiationMarrow transplantationPulmonary fibrosisMononuclear cellsProfibrotic effectsTGFβ1 geneMurine modelFibrosisTissue accumulation
2010
TGF-beta driven lung fibrosis is macrophage dependent and blocked by Serum amyloid P
Murray LA, Chen Q, Kramer MS, Hesson DP, Argentieri RL, Peng X, Gulati M, Homer RJ, Russell T, van Rooijen N, Elias JA, Hogaboam CM, Herzog EL. TGF-beta driven lung fibrosis is macrophage dependent and blocked by Serum amyloid P. The International Journal Of Biochemistry & Cell Biology 2010, 43: 154-162. PMID: 21044893, DOI: 10.1016/j.biocel.2010.10.013.Peer-Reviewed Original ResearchConceptsSerum amyloid PAnti-fibrotic effectsLung fibrosisFibrocyte accumulationAmyloid PAberrant extracellular matrix (ECM) depositionTransgenic mouse modelM2 macrophage differentiationPleiotropic growth factorExtracellular matrix depositionAirway inflammationIPF patientsAirway remodelingPulmonary fibrosisMacrophage accumulationLung diseaseLiposomal clodronateCXCL10 expressionM2 macrophagesMonocyte responsePulmonary macrophagesMouse modelCollagen depositionPathogenic mechanismsDisease severityCirculating monocytes from systemic sclerosis patients with interstitial lung disease show an enhanced profibrotic phenotype
Mathai SK, Gulati M, Peng X, Russell TR, Shaw AC, Rubinowitz AN, Murray LA, Siner JM, Antin-Ozerkis DE, Montgomery RR, Reilkoff RA, Bucala RJ, Herzog EL. Circulating monocytes from systemic sclerosis patients with interstitial lung disease show an enhanced profibrotic phenotype. Laboratory Investigation 2010, 90: 812-823. PMID: 20404807, PMCID: PMC3682419, DOI: 10.1038/labinvest.2010.73.Peer-Reviewed Original ResearchConceptsInterstitial lung diseaseSSc-ILD patientsSSc-ILDIL-10Normal controlsProfibrotic cellsSystemic sclerosisLung diseaseCollagen-producing cellsMCP-1Profibrotic phenotypeSSc-related interstitial lung diseaseFlow cytometryPeripheral blood profilesSSc-ILD cohortsIL-10 secretionSystemic sclerosis patientsExpression of CD163Blood of patientsHealthy aged controlsCultured CD14Profibrotic characteristicsProfibrotic mediatorsTNF levelsSclerosis patientsSerum Amyloid P Therapeutically Attenuates Murine Bleomycin-Induced Pulmonary Fibrosis via Its Effects on Macrophages
Murray LA, Rosada R, Moreira AP, Joshi A, Kramer MS, Hesson DP, Argentieri RL, Mathai S, Gulati M, Herzog EL, Hogaboam CM. Serum Amyloid P Therapeutically Attenuates Murine Bleomycin-Induced Pulmonary Fibrosis via Its Effects on Macrophages. PLOS ONE 2010, 5: e9683. PMID: 20300636, PMCID: PMC2837381, DOI: 10.1371/journal.pone.0009683.Peer-Reviewed Original ResearchMeSH KeywordsAgedAnimalsBleomycinCollagenFemaleFibrosisHumansLungLung DiseasesMacrophagesMaleMiceMiddle AgedPulmonary FibrosisSerum Amyloid P-ComponentConceptsSerum amyloid PPulmonary fibrosisAmyloid PIPF/UIP patientsBleomycin-Induced Pulmonary FibrosisIP10/CXCL10Fibrotic lung diseaseAberrant collagen depositionRole of macrophagesM2 macrophage phenotypeUIP patientsLung diseaseM2 macrophagesCollagen depositionTissue fibrosisMacrophage activationMacrophage phenotypeFcgamma receptorsMacrophage responsePentraxin familyTherapeutic actionFibrosisMacrophagesLungTissue remodeling