2025
ENaC contributes to macrophage dysfunction in cystic fibrosis
Moran J, Pugh C, Brown N, Thomas A, Zhang S, McCauley E, Cephas A, Shrestha C, Partida-Sanchez S, Bai S, Bruscia E, Kopp B. ENaC contributes to macrophage dysfunction in cystic fibrosis. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2025, 329: l61-l69. PMID: 40454714, PMCID: PMC12181047, DOI: 10.1152/ajplung.00009.2025.Peer-Reviewed Original ResearchConceptsCystic fibrosis transmembrane conductance regulatorCystic fibrosis transmembrane conductance regulator modulatorsMonocyte-derived macrophagesEpithelial sodium channelTransmembrane conductance regulatorCystic fibrosisImmune cellsProinflammatory cytokine productionENaC modulationENaC expressionConductance regulatorCystic fibrosis transmembrane conductance regulator inhibitionCytokine productionSodium channelsCF airway epithelial cellsReduced proinflammatory cytokine productionDecreased proinflammatory cytokine productionSodium channel expressionInfection controlTherapeutic targetAirway epithelial cellsIon channel dysfunctionReactive oxygen speciesIon channelsCFTR expressionHypercholesterolemia-induced LXR signaling in smooth muscle cells contributes to vascular lesion remodeling and visceral function
Zhang H, de Urturi D, Fernández-Tussy P, Huang Y, Jovin D, Zhang X, Huang S, Lek M, da Silva Catarino J, Sternak M, Citrin K, Swirski F, Gustafsson J, Greif D, Esplugues E, Biwer L, Suárez Y, Fernández-Hernando C. Hypercholesterolemia-induced LXR signaling in smooth muscle cells contributes to vascular lesion remodeling and visceral function. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2417512122. PMID: 40035761, PMCID: PMC11912459, DOI: 10.1073/pnas.2417512122.Peer-Reviewed Original ResearchConceptsVascular smooth muscle cellsSmooth muscle cellsLiver X receptorLesion remodelingMuscle cellsVascular functionArterial media layerContribution of lipid metabolismPhenotypic switchingRegulate vascular toneMonocyte-derived macrophagesLipid metabolismPhenotypic switching of vascular smooth muscle cellsSwitching of vascular smooth muscle cellsNecrotic core areaRegulate vascular functionFoam cell populationVisceral myopathyBladder remodelingAortic atheromaFibrous cap thicknessRemodeling in vivoLipid malabsorptionVascular toneAbundant cell typeDeletion of sphingosine 1-phosphate receptor 1 in myeloid cells reduces hepatic inflammatory macrophages and attenuates MASH
Parthasarathy G, Venkatesan N, Sidhu G, Song M, Liao C, Barrow F, Mauer A, Sehrawat T, Nakao Y, Daniel P, Dasgupta D, Pavelko K, Revelo X, Malhi H. Deletion of sphingosine 1-phosphate receptor 1 in myeloid cells reduces hepatic inflammatory macrophages and attenuates MASH. Hepatology Communications 2025, 9: e0613. PMID: 39899672, DOI: 10.1097/hc9.0000000000000613.Peer-Reviewed Original ResearchConceptsMyeloid cellsMonocyte-derived macrophagesHigh-fatLiver injuryProinflammatory monocyte-derived macrophagesReceptor 1Cell-specific knockout miceMass cytometryT cell subsetsSphingosine 1-phosphate receptor 1Cardiometabolic risk factorsS1P receptor 1Accumulation of monocyte-derived macrophagesImmune cell typesWild-typeLiver inflammatory infiltrationGene ontology pathway analysisWild-type controlsDevelopment of steatohepatitisSphingosine 1-phosphateMitogen-activated protein kinase pathwayT cellsIntrahepatic macrophagesInflammatory infiltrateKnockout mice
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 infectionDissecting the immune cell niche in pulmonary sarcoidosis – CXCL10+ monocyte-derived macrophages are potential drivers of TH17.1 inflammation
Ruwisch J, Schupp J, Bartkute B, Artysh N, Kaminski N, Prasse A. Dissecting the immune cell niche in pulmonary sarcoidosis – CXCL10+ monocyte-derived macrophages are potential drivers of TH17.1 inflammation. 2024, oa953. DOI: 10.1183/13993003.congress-2024.oa953.Peer-Reviewed Original ResearchNoninvasive assessment of the lung inflammation-fibrosis axis by targeted imaging of CMKLR1
Mannes P, Adams T, Farsijani S, Barnes C, Latoche J, Day K, Nedrow J, Ahangari F, Kaminski N, Lee J, Tavakoli S. Noninvasive assessment of the lung inflammation-fibrosis axis by targeted imaging of CMKLR1. Science Advances 2024, 10: eadm9817. PMID: 38896611, PMCID: PMC11186491, DOI: 10.1126/sciadv.adm9817.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisFibrotic lung diseaseRisk stratificationMurine modelLung fibrosisLung diseaseModel of bleomycin-induced lung fibrosisBleomycin-induced lung fibrosisImaging biomarkersMurine model of bleomycin-induced lung fibrosisBronchoalveolar lavage cellsMonocyte-derived macrophagesPositron emission tomographyInflammatory endotypesPulmonary fibrosisLavage cellsPoor survivalNoninvasive assessmentTherapeutic monitoringEmission tomographyCMKLR1FibrosisClinical trajectoryLungLung regionsResident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia
Weinberger T, Denise M, Joppich M, Fischer M, Rodriguez C, Kumaraswami K, Wimmler V, Ablinger S, Räuber S, Fang J, Liu L, Liu H, Winterhalter J, Lichti J, Thomas L, Esfandyari D, Percin G, Matin S, Hidalgo A, Waskow C, Engelhardt S, Todica A, Zimmer R, Pridans C, Perdiguero E, Schulz C. Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia. ELife 2024, 12: rp89377. PMID: 38775664, PMCID: PMC11111219, DOI: 10.7554/elife.89377.Peer-Reviewed Original ResearchConceptsInfarct sizeCardiac remodelingI/R injuryMacrophage populationsDeterioration of cardiac functionRecruitment of monocyte-derived macrophagesIschemia/reperfusion (I/R) injuryAntigen-presenting macrophagesImmune cell crosstalkSubsets of macrophagesIncreased infarct sizeMonocyte-derived macrophagesResponse to injuryInfluence infarct sizeContext of myocardial infarctionCSF1R inhibitionCardiac healingCardiac macrophagesCardiac functionCell crosstalkAdverse remodelingResident macrophagesTissue macrophagesMacrophage lineageMyocardial ischemiaResident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia
Weinberger T, Denise M, Joppich M, Fischer M, Garcia Rodriguez C, Kumaraswami K, Wimmler V, Ablinger S, Räuber S, Fang J, Liu L, Liu W, Winterhalter J, Lichti J, Thomas L, Esfandyari D, Percin G, Matin S, Hidalgo A, Waskow C, Engelhardt S, Todica A, Zimmer R, Pridans C, Gomez Perdiguero E, Schulz C. Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia. ELife 2024, 12 DOI: 10.7554/elife.89377.4.Peer-Reviewed Original ResearchInfarct sizeCardiac remodelingI/R injuryMacrophage populationsDeterioration of cardiac functionRecruitment of monocyte-derived macrophagesIschemia/reperfusion (I/R) injuryAntigen-presenting macrophagesImmune cell crosstalkSubsets of macrophagesIncreased infarct sizeMonocyte-derived macrophagesResponse to injuryInfluence infarct sizeContext of myocardial infarctionCSF1R inhibitionCardiac healingCardiac macrophagesCardiac functionCell crosstalkAdverse remodelingResident macrophagesTissue macrophagesMacrophage lineageMyocardial ischemiaAlveolar Type 2 Cells With Impaired Proteostasis Signal to Monocyte-derived Macrophages Via a MIF/DDT-CD74 Signaling Network to Promotes Pulmonary Fibrosis in IPF
Kim S, Nouws J, Cooley J, Ahangari F, Leng L, Elias J, Kaminski N, Lee P, Redente E, Kang M, Sun H, Herzog E, Bucala R, Prasse A, Sauler M. Alveolar Type 2 Cells With Impaired Proteostasis Signal to Monocyte-derived Macrophages Via a MIF/DDT-CD74 Signaling Network to Promotes Pulmonary Fibrosis in IPF. 2024, a3001-a3001. DOI: 10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a3001.Peer-Reviewed Original ResearchAlveolar type 2 cellsMonocyte-derived macrophagesType 2 cellsPromote pulmonary fibrosisPulmonary fibrosisCXCL10+ Monocyte-derived Macrophages Are Potential Drivers of TH17.1 Inflammation in Pulmonary Sarcoidosis
Ruwisch J, Schupp J, Bartkute B, Artysh N, Kaminski N, Prasse A. CXCL10+ Monocyte-derived Macrophages Are Potential Drivers of TH17.1 Inflammation in Pulmonary Sarcoidosis. 2024, a2510-a2510. DOI: 10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a2510.Peer-Reviewed Original ResearchMonocyte-derived macrophagesPulmonary sarcoidosis
2023
Trained immunity induced by high‐salt diet impedes stroke recovery
Lin T, Jiang D, Chen W, Lin J, Zhang X, Chen C, Hsu C, Lai L, Chen P, Yang K, Sansing L, Chang C. Trained immunity induced by high‐salt diet impedes stroke recovery. EMBO Reports 2023, 24: e57164. PMID: 37965920, PMCID: PMC10702837, DOI: 10.15252/embr.202357164.Peer-Reviewed Original ResearchConceptsInnate immune memoryMonocyte-derived macrophagesStroke recoveryInflammatory responseBone marrowImmune memoryHigh-salt dietCause of morbidityInitial inflammatory responsePotential therapeutic targetLoss of Nr4a1Stroke outcomeStroke brainIntracerebral hemorrhageBrain recoverySterile inflammationHealthy miceTissue injurySevere formTherapeutic targetAlternative activationImmune primingReparative functionsProgenitor cellsNR4A familyVISTA (PD-1H) Is a Crucial Immune Regulator to Limit Pulmonary Fibrosis.
Kim S, Adams T, Hu Q, Shin H, Chae G, Lee S, Sharma L, Kwon H, Lee F, Park H, Huh W, Manning E, Kaminski N, Sauler M, Chen L, Song J, Kim T, Kang M. VISTA (PD-1H) Is a Crucial Immune Regulator to Limit Pulmonary Fibrosis. American Journal Of Respiratory Cell And Molecular Biology 2023, 69: 22-33. PMID: 36450109, PMCID: PMC10324045, DOI: 10.1165/rcmb.2022-0219oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisPulmonary fibrosisImmune regulatorsTherapeutic potentialHuman idiopathic pulmonary fibrosisCrucial immune regulatorsNovel immune regulatorPulmonary fibrosis micePulmonary fibrosis modelNovel therapeutic targetRole of VISTAWild-type littermatesMonocyte-derived macrophagesT lymphocyte lineageVISTA expressionIPF treatmentAntibody treatmentImmune landscapeFibrotic mediatorsLung fibrosisFibrosis miceInflammatory responseFibrosis modelMyeloid populationsTherapeutic targetAn integrated cell atlas of the lung in health and disease
Sikkema L, Ramírez-Suástegui C, Strobl D, Gillett T, Zappia L, Madissoon E, Markov N, Zaragosi L, Ji Y, Ansari M, Arguel M, Apperloo L, Banchero M, Bécavin C, Berg M, Chichelnitskiy E, Chung M, Collin A, Gay A, Gote-Schniering J, Hooshiar Kashani B, Inecik K, Jain M, Kapellos T, Kole T, Leroy S, Mayr C, Oliver A, von Papen M, Peter L, Taylor C, Walzthoeni T, Xu C, Bui L, De Donno C, Dony L, Faiz A, Guo M, Gutierrez A, Heumos L, Huang N, Ibarra I, Jackson N, Kadur Lakshminarasimha Murthy P, Lotfollahi M, Tabib T, Talavera-López C, Travaglini K, Wilbrey-Clark A, Worlock K, Yoshida M, van den Berge M, Bossé Y, Desai T, Eickelberg O, Kaminski N, Krasnow M, Lafyatis R, Nikolic M, Powell J, Rajagopal J, Rojas M, Rozenblatt-Rosen O, Seibold M, Sheppard D, Shepherd D, Sin D, Timens W, Tsankov A, Whitsett J, Xu Y, Banovich N, Barbry P, Duong T, Falk C, Meyer K, Kropski J, Pe’er D, Schiller H, Tata P, Schultze J, Teichmann S, Misharin A, Nawijn M, Luecken M, Theis F. An integrated cell atlas of the lung in health and disease. Nature Medicine 2023, 29: 1563-1577. PMID: 37291214, PMCID: PMC10287567, DOI: 10.1038/s41591-023-02327-2.Peer-Reviewed Original ResearchConceptsCell atlasGene modulesCell typesCell type definitionsHuman Cell AtlasSingle-cell technologiesSingle-cell datasetsUndescribed cell typeMultiple lung diseasesCell statesMarker genesMonocyte-derived macrophagesDistal axisStudy of diseasesHuman tissuesAnnotationAtlasGenesSPP1DiversityExpressionTreesLimited numberCellsNew data
2022
Cellular Heterogeneity and Molecular Reprogramming of the Host Response during Influenza Acute Lung Injury
Guo K, Yombo D, Schmit T, Wang Z, Navaeiseddighi Z, Sathish V, Mathur R, Wu M, De Kumar B, Hur J, Khan N. Cellular Heterogeneity and Molecular Reprogramming of the Host Response during Influenza Acute Lung Injury. Journal Of Virology 2022, 96: e01246-22. PMID: 36286482, PMCID: PMC9645213, DOI: 10.1128/jvi.01246-22.Peer-Reviewed Original ResearchConceptsAcute lung injuryLung injuryIAV infectionHost responseDysregulated host responseExuberant host responseOutcome of interferonTotal immune cellsMonocyte-derived macrophagesSingle-cell RNA sequencing analysisChemokine responsesAcute injuryCellular levelImmune cellsNonimmune cellsBarrier integrityMyeloid cellsTherapeutic interventionsCellular heterogeneityInjuryChemokine signalingNonhematopoietic cellsInfectionRNA sequencing analysisMechanistic association
2021
Divergent Functions of Tissue-Resident and Blood-Derived Macrophages in the Hemorrhagic Brain
Chang CF, Goods BA, Askenase MH, Beatty HE, Osherov A, DeLong JH, Hammond MD, Massey J, Landreneau M, Love JC, Sansing LH. Divergent Functions of Tissue-Resident and Blood-Derived Macrophages in the Hemorrhagic Brain. Stroke 2021, 52: 1798-1808. PMID: 33840225, PMCID: PMC8085165, DOI: 10.1161/strokeaha.120.032196.Peer-Reviewed Original ResearchConceptsMonocyte-derived macrophagesIntracerebral hemorrhageT cell proliferationCore transcriptional programDifferential gene expressionDistinct transcriptional signaturesBone marrow-derived macrophagesAntigen-specific T cell proliferationTranscriptional programsCD4 T cell proliferationLongitudinal transcriptomic analysisVivo phagocytosis assaysTranscriptomic analysisDivergent functionsMarrow-derived macrophagesMHCII genesTissue-resident microgliaAntigen-presenting capabilityAutologous blood injectionGene expressionPrimary microglia culturesInnate immune cellsPhagocytosis of debrisTranscriptional signatureBlood-derived macrophages
2020
Single-Cell Transcriptional Archetypes of Airway Inflammation in Cystic Fibrosis.
Schupp JC, Khanal S, Gomez JL, Sauler M, Adams TS, Chupp GL, Yan X, Poli S, Zhao Y, Montgomery RR, Rosas IO, Dela Cruz CS, Bruscia EM, Egan ME, Kaminski N, Britto CJ. Single-Cell Transcriptional Archetypes of Airway Inflammation in Cystic Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2020, 202: 1419-1429. PMID: 32603604, PMCID: PMC7667912, DOI: 10.1164/rccm.202004-0991oc.Peer-Reviewed Original ResearchConceptsCF lung diseaseHealthy control subjectsImmune dysfunctionLung diseaseCystic fibrosisControl subjectsSputum cellsAbnormal chloride transportLung mononuclear phagocytesInnate immune dysfunctionDivergent clinical coursesImmune cell repertoireMonocyte-derived macrophagesCF monocytesAirway inflammationClinical courseProinflammatory featuresCell survival programInflammatory responseTissue injuryCell repertoireImmune functionTranscriptional profilesAlveolar macrophagesMononuclear phagocytesIRE1A Stimulates Hepatocyte-Derived Extracellular Vesicles That Promote Inflammation in Mice With Steatohepatitis
Dasgupta D, Nakao Y, Mauer A, Thompson J, Sehrawat T, Liao C, Krishnan A, Lucien F, Guo Q, Liu M, Xue F, Fukushima M, Katsumi T, Bansal A, Pandey M, Maiers J, DeGrado T, Ibrahim S, Revzin A, Pavelko K, Barry M, Kaufman R, Malhi H. IRE1A Stimulates Hepatocyte-Derived Extracellular Vesicles That Promote Inflammation in Mice With Steatohepatitis. Gastroenterology 2020, 159: 1487-1503.e17. PMID: 32574624, PMCID: PMC7666601, DOI: 10.1053/j.gastro.2020.06.031.Peer-Reviewed Original ResearchConceptsX-box binding protein 1Release of EVsHepatocyte-derived extracellular vesiclesSerine palmitoyltransferase genesExtracellular vesiclesSerine palmitoyltransferaseChromatin immunoprecipitationCeramide biosynthesisInflammatory Extracellular VesiclesMonocyte-derived macrophagesUnfolded protein responseNonalcoholic steatohepatitisDiet-induced steatohepatitisGene expression analysisPrimary hepatocytesNumber of EVsBinding protein 1Cultured primary hepatocytesNanoparticle-tracking analysisNanoscale flow cytometryIRE1ALiver tissueRate-limiting enzymeProtein responseExpression analysisProfibrotic Activation of Human Macrophages in Systemic Sclerosis
Bhandari R, Ball MS, Martyanov V, Popovich D, Schaafsma E, Han S, ElTanbouly M, Orzechowski NM, Carns M, Arroyo E, Aren K, Hinchcliff M, Whitfield ML, Pioli PA. Profibrotic Activation of Human Macrophages in Systemic Sclerosis. Arthritis & Rheumatology 2020, 72: 1160-1169. PMID: 32134204, PMCID: PMC7329566, DOI: 10.1002/art.41243.Peer-Reviewed Original ResearchMeSH KeywordsAdultAntigens, CDAntigens, Differentiation, MyelomonocyticCell DifferentiationChemokine CCL2Coculture TechniquesFemaleFibroblastsFibrosisHLA-DR AntigensHumansImmunophenotypingInterleukin-6Lectins, C-TypeLeukocytes, MononuclearMacrophage ActivationMacrophagesMaleMannose ReceptorMannose-Binding LectinsMiddle AgedMonocytesPhosphorylationReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IIReceptors, Cell SurfaceRNA, MessengerScleroderma, SystemicSkinSTAT3 Transcription FactorTranscriptomeTransforming Growth Factor betaConceptsPeripheral blood mononuclear cellsSystemic sclerosisSSc patientsBasal conditionsSex-matched healthy controlsSSc fibroblastsSurface markersHealthy donor monocytesBlood mononuclear cellsMediator of fibrosisInflammatory macrophage activationMonocyte-derived macrophagesActivation profilesGrowth factor βFibrotic activationGene expression signaturesDonor monocytesMononuclear cellsProfibrotic activationSkin fibrosisInterleukin-6Healthy controlsSSc skinIndependent cohortMacrophage activation
2019
IL23 induces IL23R recycling and amplifies innate receptor-induced signalling and cytokines in human macrophages, and the IBD-protective IL23R R381Q variant modulates these outcomes
Sun R, Hedl M, Abraham C. IL23 induces IL23R recycling and amplifies innate receptor-induced signalling and cytokines in human macrophages, and the IBD-protective IL23R R381Q variant modulates these outcomes. Gut 2019, 69: 264-273. PMID: 31097538, PMCID: PMC6858485, DOI: 10.1136/gutjnl-2018-316830.Peer-Reviewed Original ResearchConceptsMonocyte-derived macrophagesHuman monocyte-derived macrophagesJanus kinase/signal transducerKinase/signal transducerDynamin-mediated endocytosisReceptor-induced signalingCell surface regulationR381Q variantIBD pathogenesisIntestinal myeloid cellsLate endosomesPattern recognition receptorsSignal transducerPathway membersDefines mechanismsReal-time PCRCell typesHeLa cellsSignalingKey playersRNA expressionHuman macrophagesPathwayWestern blotMyeloid cells
2017
Erythrocyte efferocytosis modulates macrophages towards recovery after intracerebral hemorrhage
Chang CF, Goods BA, Askenase MH, Hammond MD, Renfroe SC, Steinschneider AF, Landreneau MJ, Ai Y, Beatty HE, da Costa LHA, Mack M, Sheth KN, Greer DM, Huttner A, Coman D, Hyder F, Ghosh S, Rothlin CV, Love JC, Sansing LH. Erythrocyte efferocytosis modulates macrophages towards recovery after intracerebral hemorrhage. Journal Of Clinical Investigation 2017, 128: 607-624. PMID: 29251628, PMCID: PMC5785262, DOI: 10.1172/jci95612.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisAxl Receptor Tyrosine KinaseBrain Injuriesc-Mer Tyrosine KinaseCerebral HemorrhageErythrocytesHematomaHumansImmunity, InnateInflammationMacrophagesMaleMiceMice, Inbred C57BLMice, TransgenicPhagocytosisPhenotypeProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesSolubilityTreatment OutcomeConceptsMonocyte-derived macrophagesIntracerebral hemorrhageEryptotic erythrocytesNeurological recoveryHematoma clearanceExperimental intracerebral hemorrhageReceptor tyrosine kinase AXLHuman monocyte-derived macrophagesTyrosine kinase AXLICH onsetFunctional outcomeBrain injuryTissue injurySoluble AxlDynamic phenotypic changesAlternative activationPhenotypic changesMacrophage phenotypeIron depositionMurine brainMacrophage responseRestorative functionEfferocytosisMacrophagesEngulfment of erythrocytes
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply