2025
Endothelial CLEC5A drives barrier dysfunction and vascular leakage responsible for lung injury in bacterial pneumonia and sepsis
Zhang T, Huang X, Goodwin J, Wen R, Liu Y, Yang Y, Zhang T, Zheng Y, Chen A, Hao P, Tong X, Yang N, Liu C. Endothelial CLEC5A drives barrier dysfunction and vascular leakage responsible for lung injury in bacterial pneumonia and sepsis. Science Advances 2025, 11: eadt7589. PMID: 40498836, PMCID: PMC12154197, DOI: 10.1126/sciadv.adt7589.Peer-Reviewed Original ResearchConceptsVascular leakagePuncture (CLP)-induced polymicrobial sepsisRegulating endothelial barrier functionCLP-challenged miceEndothelial barrier dysfunctionTrans-endothelial electrical resistanceEndothelial barrier functionLipopolysaccharide (LPS)-induced endotoxemiaVascular endothelial cellsPattern recognition receptorsSurvival benefitMultiorgan failurePolymicrobial sepsisTrans-endothelial migrationCecal ligationBacterial pneumoniaLung injuryBarrier dysfunctionVascular injurySingle-cell RNA sequencingDecreased mortalityInflammatory stormBacterial infectionsHeterogeneity of vascular endothelial cellsSepsisSeparation of telomere protection from length regulation by two different point mutations at amino acid 492 of RTEL1
Smoom R, May C, Lichtental D, Bar-Ness K, Rangel R, Khoury J, Nachmani D, Avrahami D, Ahangari F, Skordalakes E, Kaminski N, Kaestner K, Tzfati Y. Separation of telomere protection from length regulation by two different point mutations at amino acid 492 of RTEL1. Nucleic Acids Research 2025, 53: gkaf507. PMID: 40530700, PMCID: PMC12203905, DOI: 10.1093/nar/gkaf507.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SubstitutionAnimalsDisease Models, AnimalDNA DamageDNA HelicasesDyskeratosis CongenitaFetal Growth RetardationGrowth DisordersHematopoiesisHumansIntellectual DisabilityLimb Deformities, CongenitalLungMiceMicrocephalyPoint MutationTelomereTelomere HomeostasisX-Linked Intellectual DisabilityConceptsHoyeraal-Hreidarsson syndromeTelomere protectionLength regulationTelomere length regulationTelomere-related diseasesTelomere biology disordersDNA helicaseMouse genomeGenome stabilityMouse modelMouse telomeresAberrant hematopoiesisGenomic instabilityPoint mutationsHouse miceTelomeric DNA damageAnaphase bridgesRTEL1Amino acidsTelomereMechanistic rolesDNA damageMutationsIsoleucine mutationGenomeSmall Cell Lung Cancer
Kim S, Park H, Chiang A. Small Cell Lung Cancer. JAMA 2025, 333: 1906-1917. PMID: 40163214, DOI: 10.1001/jama.2025.0560.Peer-Reviewed Original ResearchConceptsSmall cell lung cancerFirst-line treatmentCell lung cancerES-SCLCLS-SCLCLung cancerPlatinum-etoposideMaintenance immunotherapyOverall survivalMedian overall survival of patientsCell death 1 ligand 1Programmed cell death 1 ligand 1Rate of tumor shrinkageHigh-grade neuroendocrine carcinomaThree-year overall survivalBispecific T-cell engagerDelta-like ligand 3Overall survival of patientsDevelopment of small cell lung cancerPlatinum-etoposide chemotherapyPrimary lung massMedian overall survivalSecond-line therapyT-cell engagersSmoking-related malignanciesIL‐6 signaling regulates the inflammatory response without impacting pathogen burden during influenza‐associated pulmonary aspergillosis
Sharma L, Singh R, Tolman N, Ngeow C, Duray A, Naghshtabrizi N, Ahmad A, Bain W, Robinson K. IL‐6 signaling regulates the inflammatory response without impacting pathogen burden during influenza‐associated pulmonary aspergillosis. Physiological Reports 2025, 13: e70372. PMID: 40420617, PMCID: PMC12106949, DOI: 10.14814/phy2.70372.Peer-Reviewed Original ResearchConceptsAF infectionAspergillus fumigatusInterleukin-6IL-6 signalingLung inflammationInfluenza-associated pulmonary aspergillosisInterleukin-6 knockout miceNeutrophilic lung inflammationBronchoalveolar lavage fluidEpithelial cell damageLung capillary permeabilitySusceptibility to opportunistic pathogensPulmonary aspergillosisClinical courseLavage fluidKnockout miceOpportunistic pathogenRAGE levelsEpithelial integrityMouse modelIL-6Pathological inflammationTissue injuryInflammatory responseViral infectionTranscriptional signatures of endothelial cells shape immune responses in cardiopulmonary health and disease
Fließer E, Jandl K, Chen S, Wang M, Schupp J, Kuebler W, Baker A, Kwapiszewska G. Transcriptional signatures of endothelial cells shape immune responses in cardiopulmonary health and disease. JCI Insight 2025, 10: e191059. PMID: 40401523, PMCID: PMC12128986, DOI: 10.1172/jci.insight.191059.Peer-Reviewed Original ResearchConceptsEndothelial cellsCardiopulmonary vasculatureImmune responseImmune cell recruitmentRegulation of immune responsesFunction of endothelial cellsImmunoregulatory roleAntigen presentationCytokine secretionCell recruitmentCardiopulmonary healthDelivery of oxygenSingle-cell RNA sequencingImmunomodulatory propertiesCardiopulmonary diseaseClearance functionDisease pathogenesisTherapy targetTranscriptional signatureEC subpopulationsImmunomodulatory activityDiseaseLungVasculatureHeartMineralocorticoid receptor phase separation modulates cardiac preservation
Lei I, Sicim H, Gao W, Huang W, Noly P, Pergande M, Wilson M, Lee A, Liu L, Abou El Ela A, Jiang M, Saddoughi S, Pober J, Platt J, Cascalho M, Pagani F, Chen Y, Pitt B, Wang Z, Mortensen R, Ge Y, Tang P. Mineralocorticoid receptor phase separation modulates cardiac preservation. Nature Cardiovascular Research 2025, 4: 710-726. PMID: 40389663, DOI: 10.1038/s44161-025-00653-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell Cycle ProteinsCold IschemiaHeart TransplantationHistone Deacetylase 1HumansKidneyLiverLungMaleMiceMice, Inbred C57BLMineralocorticoid Receptor AntagonistsMyocytes, CardiacNuclear ProteinsOrgan PreservationPhase SeparationReceptors, MineralocorticoidTissue DonorsTranscription FactorsConceptsMineralocorticoid receptorDonor heartsHistone deacetylase 1Bromodomain-containing 4Gold standard treatmentEnd-stage heart failureCold ischemic timeShortage of donor heartsExpressed MRDonor cardiomyocytesHuman donor heartsHeart transplantationStandard treatmentIschemic timeHeart failureCardiac preservationSolid organsPharmacological inhibitionCold preservationPreserving biologyHeartYou know my NAMs
Ghosh S, Rothlin C. You know my NAMs. Immunity 2025, 58: 1179-1181. PMID: 40367920, DOI: 10.1016/j.immuni.2025.04.025.Peer-Reviewed Original ResearchArtificial Intelligence–Guided Lung Ultrasound by Nonexperts
Baloescu C, Bailitz J, Cheema B, Agarwala R, Jankowski M, Eke O, Liu R, Nomura J, Stolz L, Gargani L, Alkan E, Wellman T, Parajuli N, Marra A, Thomas Y, Patel D, Schraft E, O’Brien J, Moore C, Gottlieb M. Artificial Intelligence–Guided Lung Ultrasound by Nonexperts. JAMA Cardiology 2025, 10: 245-253. PMID: 39813064, PMCID: PMC11904735, DOI: 10.1001/jamacardio.2024.4991.Peer-Reviewed Original ResearchThis study shows AI helps non-experts create expert-quality lung ultrasound images, which may improve healthcare diagnostics access in underserved areas.Association between Organochlorine Exposures and Lung Functions Modified by Thyroid Hormones and Mediated by Inflammatory Factors among Healthy Older Adults
Guo X, Ren H, Zhang J, Ma X, Tong S, Tang S, Mao C, Shi X. Association between Organochlorine Exposures and Lung Functions Modified by Thyroid Hormones and Mediated by Inflammatory Factors among Healthy Older Adults. Biomedical And Environmental Sciences 2025, 38: 144-153. PMID: 40159168, DOI: 10.3967/bes2025.015.Peer-Reviewed Original ResearchConceptsLung functionInflammatory factorsIL-13Hormone groupThyroid hormonesEffects of IL-2Organochlorine exposureHealthy older adultsInterleukin (IL)-2Thyroid hormone levelsAssociated with forced vital capacityOlder adultsForced vital capacityIL-7IL-2Hormone levelsIL-8Wearable passive samplersEffects of organochlorinesAssociated with changesVital capacityLungMediation analysisParticipants' lung functionBlood samplesEpigenetic age acceleration in idiopathic pulmonary fibrosis revealed by DNA methylation clocks
Kurbanov D, Ahangari F, Adams T, De Man R, Tang J, Carlon M, Abu Hussein N, Cortesi E, Zapata M, De Sadelaar L, Wuyts W, Vanaudenaerde B, Kaminski N, McDonough J. Epigenetic age acceleration in idiopathic pulmonary fibrosis revealed by DNA methylation clocks. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2025, 328: l456-l462. PMID: 39970931, PMCID: PMC12169420, DOI: 10.1152/ajplung.00171.2024.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisIdiopathic pulmonary fibrosis tissuePulmonary fibrosisLung tissueEpigenetic clocksPotential of DNA methylationDNA methylation levelsDebilitating lung diseaseIllumina MethylationEPIC arrayHuman lung tissueEpigenetic ageDNA methylation clocksBiological ageAffected lung tissueIPF casesClinical prognosisMethylation patternsDNA methylationLung diseaseHealthy controlsAcceleration of biological agingMethylation levelsMethylationEPIC arrayAge accelerationClinical assessmentCD103+ dendritic cell — fibroblast crosstalk via TLR9, TDO2, and AHR signaling drives lung fibrogenesis
Carter H, Costa R, Adams T, Gilchrist T, Emch C, Bame M, Oldham J, Huang S, Linderholm A, Noth I, Kaminski N, Moore B, Gurczynski S. CD103+ dendritic cell — fibroblast crosstalk via TLR9, TDO2, and AHR signaling drives lung fibrogenesis. JCI Insight 2025, 10 PMID: 39964756, PMCID: PMC11949071, DOI: 10.1172/jci.insight.177072.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDBasic Helix-Loop-Helix Transcription FactorsBleomycinDendritic CellsDisease Models, AnimalFibroblastsHumansIdiopathic Pulmonary FibrosisIntegrin alpha ChainsInterleukin-6LungMaleMiceMice, Inbred C57BLReceptors, Aryl HydrocarbonSignal TransductionToll-Like Receptor 9Tryptophan OxygenaseConceptsIdiopathic pulmonary fibrosisAhR signalingMice treated with BLMIL-17+ cellsCD103+ DCLoss of lung functionStudies of human samplesLimited treatment optionsTreated ex vivoProduction of IL-6Inflammatory cytokine productionExon 2 deletionExpression of TDO2IL-6 productionAdoptive transferCD11c-CreCD11c+ cellsImmunological changesPulmonary fibrosisTLR agonistsProgressive scarringTreatment optionsCytokine productionLung fibrogenesisAryl hydrocarbon receptorStandard to Handheld: A New Wave in Thoracic Ultrasound and Patient Care—A Direct Comparison of Portable Handheld Against Standard in Thoracic Ultrasound
Halim D, Kelly A, Hayes J, Bennett K, Tzouvelekis A, Ampazis D, Sampsonas F. Standard to Handheld: A New Wave in Thoracic Ultrasound and Patient Care—A Direct Comparison of Portable Handheld Against Standard in Thoracic Ultrasound. Medicina 2025, 61: 313. PMID: 40005430, PMCID: PMC11857366, DOI: 10.3390/medicina61020313.Peer-Reviewed Original ResearchConceptsLevels of experienceNon-inferiorityPortable ultrasound deviceOverall image qualityLung pathologyUltrasound deviceInterquartile rangeRespiratory departmentThoracic ultrasoundAnatomical visualizationHandheld ultrasound devicePatient careImprove healthcareOperator's level of experienceNo significant differenceLikert scaleTrainee levelStatistically significant variablesDiagnostic accuracyClinical decisionsOverall perceptionOnline questionnaireClinical utilityMedian rateClinical settingTherapeutic JAK inhibition does not impact lung injury during viral or bacterial pneumonia in male mice
Sharma L, Singh R, Ngeow C, van der Geest R, Duray A, Tolman N, McVerry B, Dela Cruz C, Alcorn J, Bain W, Robinson K. Therapeutic JAK inhibition does not impact lung injury during viral or bacterial pneumonia in male mice. Physiological Reports 2025, 13: e70232. PMID: 39921246, PMCID: PMC11805821, DOI: 10.14814/phy2.70232.Peer-Reviewed Original ResearchConceptsMurine model of influenzaIL-6 deletionMRSA pneumoniaModel of influenzaInflammatory cell recruitmentIL-6Interferon-stimulated genesMurine modelCell recruitmentJAK inhibitionElevated levels of IL-6Tissue injuryLevels of IL-6IL-6 deficiencyJAK inhibitor baricitinibSuppression of cytokinesLimit tissue injuryLung tissue injurySecondary bacterial infectionInfluenza infectionJAK/STAT signaling pathwayBaricitinib treatmentInhibitory therapyClinical efficacyBacterial burdenCollagen Hybridizing Peptide-Based Radiotracers for Molecular Imaging of Collagen Turnover in Pulmonary Fibrosis.
Ahmad A, Ghim M, Kukreja G, Neishabouri A, Zhang Z, Li J, Salarian M, Toczek J, Gona K, Hedayatyanfard K, Morrison T, Zhang J, Huang Y, Liu C, Yu S, Sadeghi M. Collagen Hybridizing Peptide-Based Radiotracers for Molecular Imaging of Collagen Turnover in Pulmonary Fibrosis. Journal Of Nuclear Medicine 2025, 66: 425-433. PMID: 39915119, PMCID: PMC11876730, DOI: 10.2967/jnumed.124.268832.Peer-Reviewed Original ResearchConceptsPulmonary fibrosisTracer uptakeLung uptakeMurine model of pulmonary fibrosisModel of pulmonary fibrosisMice 3 wkEffect of antifibrotic therapyCollagen turnoverInterstitial lung diseaseClinical diagnostic methodsSPECT/CT imagingHybrid tracersLung histologyAntifibrotic therapyControl miceDisease activityMurine modelLung diseaseMice 8Tissue fibrosisPatient managementLiver uptakeSPECT/CTFibrosisSPECT imagesThe fungal microbiota modulate neonatal oxygen-induced lung injury
Martin I, Silverberg M, Abdelgawad A, Tanaka K, Halloran B, Nicola T, Myers E, Desai J, White C, Karabayir I, Akbilgic O, Tipton L, Gentle S, Ambalavanan N, Peters B, Vu L, Jain V, Lal C, Cormier S, Pierre J, Jilling T, Talati A, Willis K. The fungal microbiota modulate neonatal oxygen-induced lung injury. Microbiome 2025, 13: 24. PMID: 39871397, PMCID: PMC11773857, DOI: 10.1186/s40168-025-02032-x.Peer-Reviewed Original ResearchConceptsBronchopulmonary dysplasiaLung injury severityLung injuryDevelopment of bronchopulmonary dysplasiaSeverity of lung injuryAugmented lung injuryMorbidities of prematurityVery preterm infantsOxygen-induced lung injuryChronic lung diseaseIntestinal microbiomeMicrobiome of infantsPotential therapeutic strategyPreterm infantsNeonatal microbiomePremature infantsPremature neonatesInjury severityMurine modelNeonatal healthLung diseaseMouse modelTherapeutic strategiesLoss of function approachesFungal communitiesContinued Treatment with Nintedanib in Patients with Progressive Pulmonary Fibrosis: Data from INBUILD-ON
Wuyts W, Bonella F, Chaudhuri N, Varone F, Antin-Ozerkis D, Song J, Miede C, Dumistracel M, Coeck C, Cottin V. Continued Treatment with Nintedanib in Patients with Progressive Pulmonary Fibrosis: Data from INBUILD-ON. Lung 2025, 203: 25. PMID: 39789408, PMCID: PMC11717875, DOI: 10.1007/s00408-024-00778-z.Peer-Reviewed Original ResearchConceptsProgressive pulmonary fibrosisForced vital capacityAdverse eventsSafety profilePulmonary fibrosisConclusionThe safety profileDiscontinuation of nintedanibExposure to nintedanibSafety of nintedanibOpen-label extensionBaseline to weekFrequent adverse eventsFatal adverse eventsLong-term treatmentLonger-term treatmentNintedanib groupGastrointestinal eventsINBUILD trialNintedanibMethodsAdverse eventsModerate severityPatientsContinuous treatmentVital capacityINBUILDTranscriptomic analysis reveals shared deregulated neutrophil responses in COVID-19 and idiopathic pulmonary fibrosis
Divolis G, Synolaki E, Tringidou R, Tzouvelekis A, Boumpas D, Skendros P, Galani I. Transcriptomic analysis reveals shared deregulated neutrophil responses in COVID-19 and idiopathic pulmonary fibrosis. Respiratory Research 2025, 26: 213. PMID: 40500689, PMCID: PMC12160113, DOI: 10.1186/s12931-025-03180-2.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosis patientsIdiopathic pulmonary fibrosisNeutrophil extracellular trapsPulmonary fibrosisIPF pathophysiologyPeripheral blood neutrophil countElevated peripheral blood neutrophil countsAcute respiratory distress syndromeCOVID-19 neutrophilsPeripheral blood of COVID-19 patientsLung biopsy specimensBlood of COVID-19 patientsRespiratory distress syndromeDeregulated immune responseNeutrophil extracellular trap formationBlood neutrophil countNeutrophil-driven pathologiesCOVID-19 pathogenesisCOVID-19 patientsLung biopsyBiopsy specimensDistress syndromePeripheral bloodNeutrophil countActivin/follistatin system
2024
Predicting lung aging using scRNA-Seq data
Song Q, Singh A, McDonough J, Adams T, Vos R, De Man R, Myers G, Ceulemans L, Vanaudenaerde B, Wuyts W, Yan X, Schupp J, Hagood J, Kaminski N, Bar-Joseph Z. Predicting lung aging using scRNA-Seq data. PLOS Computational Biology 2024, 20: e1012632. PMID: 39700255, PMCID: PMC11741621, DOI: 10.1371/journal.pcbi.1012632.Peer-Reviewed Original ResearchEzrin drives adaptation of monocytes to the inflamed lung microenvironment
Gudneppanavar R, Di Pietro C, H Öz H, Zhang P, Cheng E, Huang P, Tebaldi T, Biancon G, Halene S, Hoppe A, Kim C, Gonzalez A, Krause D, Egan M, Gupta N, Murray T, Bruscia E. Ezrin drives adaptation of monocytes to the inflamed lung microenvironment. Cell Death & Disease 2024, 15: 864. PMID: 39613751, PMCID: PMC11607083, DOI: 10.1038/s41419-024-07255-8.Peer-Reviewed Original ResearchConceptsActivation of focal adhesion kinaseExtracellular matrixActin-binding proteinsFocal adhesion kinaseLung extracellular matrixKnock-out mouse modelProtein kinase signalingCortical cytoskeletonLoss of ezrinKinase signalingPlasma membraneCell migrationSignaling pathwayEzrinResponse to lipopolysaccharideTissue-resident macrophagesMouse modelLipopolysaccharideCytoskeletonEzrin expressionLung microenvironmentKinaseMonocyte recruitmentProteinAktMouse Models Enable the Functional Investigation of Tertiary Lymphoid Structures in Cancer
Jeevanandam A, Yin Z, Connolly K, Joshi N. Mouse Models Enable the Functional Investigation of Tertiary Lymphoid Structures in Cancer. Methods In Molecular Biology 2024, 2864: 57-76. PMID: 39527217, DOI: 10.1007/978-1-0716-4184-2_4.Peer-Reviewed Original ResearchConceptsTertiary lymphoid structuresTertiary lymphoid structure formationSecondary lymphoid organsLymphoid structuresMurine modelFeatures of tertiary lymphoid structuresFunction of tertiary lymphoid structuresMouse modelPersistent inflammatory stimulationAssociated with positive clinical outcomesTissue-specific regulatory mechanismsPositive clinical outcomesPrognostic significanceClinical outcomesGut environmentNonlymphoid tissuesLymphoid aggregatesLymphoid organsMouse lungCancer patientsGenetic sequencesInflammatory stimulationRegulatory mechanismsTherapeutic modulationClinical efforts
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