2025
Effects of lung expansion on global and regional pulmonary blood volume in a sheep model of acute lung injury.
Zang M, Zeng C, Lagier D, Leng N, Grogg K, Motta-Ribeiro G, Laine A, Winkler T, Vidal Melo M. Effects of lung expansion on global and regional pulmonary blood volume in a sheep model of acute lung injury. Anesthesiology 2025 PMID: 39946655, DOI: 10.1097/aln.0000000000005412.Peer-Reviewed Original ResearchPositive end-expiratory pressurePulmonary blood volumeLung expansionBlood volumeLung injurySystemic endotoxemiaMechanical ventilationRespiratory-gated positron emission tomographyVentilator-induced lung injuryModel of acute lung injuryDistribution of blood volumeAcute lung injuryLow-volume mechanical ventilationLung injury modelEnd-expiratory pressureQuantify blood volumePulmonary capillary blood volumeLow blood volumeRegional blood volumePositron emission tomographyVascular blood volumeCapillary blood volumeLung blood volumeCapillary closureEnd-inspirationDamage sensing through TLR9 regulates inflammatory and antiviral responses during influenza infection
Kim J, Yuan Y, Agaronyan K, Zhao A, Wang V, Gau D, Toosi N, Gupta G, Essayas H, Kaminski A, McGovern J, Yu S, Woo S, Lee C, Gandhi S, Saber T, Saleh T, Hu B, Sun Y, Ishikawa G, Bain W, Evankovich J, Chen L, Yun H, Herzog E, Dela Cruz C, Ryu C, Sharma L. Damage sensing through TLR9 regulates inflammatory and antiviral responses during influenza infection. Mucosal Immunology 2025 PMID: 39884393, DOI: 10.1016/j.mucimm.2025.01.008.Peer-Reviewed Original ResearchToll-like receptor 9Anti-influenza immunityToll-like receptor 9 activationImpaired viral clearanceViral clearanceMyeloid cellsTissue injuryInflammatory responseInfluenza infectionPersistent inflammationLung injuryTissue damageToll-like receptor 9 deficiencyReceptor 9Toll-like receptor 9 signalingToll-like receptor 9 ligandInfection of immune cellsInfluenza-infected individualsPersistent lung injuryTLR9-/- miceInfected myeloid cellsInflammatory lung injurySensing tissue damageUnmethylated CpG DNA sequencesMitochondrial DNAThe 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 communities
2024
Factors Associated with Pediatric Drowning-Associated Lung Injury
Shenoi R, Crowe J, Dorfman S, Bergmann K, Mistry R, Hariharan S, Tavarez M, Wai S, Jones J, Langhan M, Ward C, McCallin T, Sethuraman U, Shah N, Mendez D, Wolpert K, Santos-Malave C, Ruttan T, Quayle K, Okada P, Bubolz B, Buscher J, McKee R, Mangold K, Wendt W, Thompson A, Hom J, Brayer A, Blackstone M, Brennan C, Russell W, Agarwal M, Khanna K, Louie J, Sheridan D, Camp E, Committee P. Factors Associated with Pediatric Drowning-Associated Lung Injury. The Journal Of Pediatrics 2024, 279: 114459. PMID: 39736377, DOI: 10.1016/j.jpeds.2024.114459.Peer-Reviewed Original ResearchConceptsRisk factorsEmergency departmentCross-sectional study of childrenEmergency medical servicesPediatric emergency departmentCross-sectional studyAbnormal respiratory rateLung injuryPrehospital dataSpine injuriesAbnormal chest radiographic findingsED presentationsDrowning deathsMedical servicesPatient dispositionStudy of childrenChest radiographic findingsED courseAbnormal heart rateLogistic regressionShort-term outcomesAbnormal lung auscultationChest radiograph reportsRadiographic reportsOlder ageContext‐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 recoveryPathophysiology and Prevention of Manual-Ventilation-Induced Lung Injury (MVILI)
White L, Conrad S, Alexander J. Pathophysiology and Prevention of Manual-Ventilation-Induced Lung Injury (MVILI). Pathophysiology 2024, 31: 583-595. PMID: 39449524, PMCID: PMC11503381, DOI: 10.3390/pathophysiology31040042.Peer-Reviewed Original ResearchManual ventilationLung injuryManual hyperventilationOperator-dependent skillsShort-term ventilationMechanism of injuryManikin-based studyBag valve maskAmerican Heart AssociationEuropean Resuscitation CouncilHyperventilated patientsMechanical ventilationHemodynamic alterationsHealthcare providersHeart AssociationPatient populationResuscitation effortsGastric regurgitationResuscitation CouncilCardiopulmonary resuscitationVentilation parametersPatientsInjury processAcute barotraumaVentilationProtective mechanical ventilation in critically ill patients after surgery
Zorrilla-Vaca A, Arevalo J, Grant M. Protective mechanical ventilation in critically ill patients after surgery. Current Opinion In Critical Care 2024, 30: 679-683. PMID: 39503212, DOI: 10.1097/mcc.0000000000001215.Peer-Reviewed Original ResearchIntensive care unitVentilator-induced lung injuryLung protective strategyCritically ill patientsMechanical ventilationCare unitLung injurySurgical patientsFast-track extubation protocolOpen-lung ventilation strategyIll patientsRisk of ventilator-induced lung injuryHigh-flow nasal cannulaHigh-risk surgical patientsOpen lung ventilationOperating roomNoninvasive ventilation supportProtective mechanical ventilationPositive-end expiratory pressureAcute lung injuryMechanically ventilated patientsStandard of careThoracic surgeryNasal cannulaRetrospective studyChitinase 3-like-1 Inhibits Innate Antitumor and Tissue Remodeling Immune Responses by Regulating CD47-SIRPα- and CD24-Siglec10-Mediated Phagocytosis.
Ma B, Kamle S, Sadanaga T, Lee C, Lee J, Yee D, Zhu Z, Silverman E, DeMeo D, Choi A, Lee C, Elias J. Chitinase 3-like-1 Inhibits Innate Antitumor and Tissue Remodeling Immune Responses by Regulating CD47-SIRPα- and CD24-Siglec10-Mediated Phagocytosis. The Journal Of Immunology 2024, 213: 1279-1291. PMID: 39291933, DOI: 10.4049/jimmunol.2400035.Peer-Reviewed Original ResearchImmune checkpoint moleculesChronic obstructive pulmonary diseaseInhibit adaptive immune responsesAdaptive immune responsesInnate immune responseImmune responseInhibition of innate immune responsesInhibits T cell costimulationGeneration of adaptive immune responsesMacrophage phagocytosisInhibit innate immune responsesChitinase 3-like 1T cell costimulationEpithelial cell deathObstructive pulmonary diseaseCheckpoint moleculesPoor prognosisLung injuryInhibit macrophagesPulmonary diseaseCHI3L1Inflammation pathwaysCancerSHP-2 phosphataseCell deathCasRx-based Wnt activation promotes alveolar regeneration while ameliorating pulmonary fibrosis in a mouse model of lung injury
Shen S, Wang P, Wu P, Huang P, Chi T, Xu W, Xi Y. CasRx-based Wnt activation promotes alveolar regeneration while ameliorating pulmonary fibrosis in a mouse model of lung injury. Molecular Therapy 2024, 32: 3974-3989. PMID: 39245939, PMCID: PMC11573616, DOI: 10.1016/j.ymthe.2024.09.008.Peer-Reviewed Original ResearchWnt/b-catenin signalingStem cell activityLung epitheliumAlveolar regenerationPulmonary fibrosisLung fibrosisWnt signalingCell activationMouse models of lung injuryModel of lung injuryWnt activityAlveolar type II cell proliferationBleomycin-induced injuryAmeliorated pulmonary fibrosisActivation of Wnt signalingType II cell proliferationInhibit lung fibrosisRegenerative medicineAnti-fibrotic effectsTreating pulmonary fibrosisActivated Wnt signalingLung injuryMouse modelFibrosisWnt/b-cateninAdjunctive N-Acetylcysteine and Lung Function in Pulmonary Tuberculosis.
Wallis R, Sabi I, Lalashowi J, Bakuli A, Mapamba D, Olomi W, Siyame E, Ngaraguza B, Chimbe O, Charalambous S, Rachow A, Ivanova O, Zurba L, Myombe B, Kunambi R, Hoelscher M, Ntinginya N, Churchyard G. Adjunctive N-Acetylcysteine and Lung Function in Pulmonary Tuberculosis. NEJM Evidence 2024, 3: evidoa2300332. PMID: 39189858, DOI: 10.1056/evidoa2300332.Peer-Reviewed Original ResearchConceptsWhole blood glutathione levelsLung functionN-acetylcysteinePulmonary tuberculosisCulture conversionSecondary outcomesGlutathione levelsEffect of N-acetylcysteineTuberculosis treatment outcomesOutcome of lung functionOral N-acetylcysteineRecovery of lung functionAdjunctive N-acetylcysteineAssociated with improved recoveryN-acetylcysteine treatmentPermanent lung injuryFar-advanced tuberculosisSputum cultureStandard therapyNAC administrationAdverse eventsLung injuryGlobal health concernCohort studyClinical evaluationMechanical ventilation guided by driving pressure optimizes local pulmonary biomechanics in an ovine model
Lagier D, Zeng C, Kaczka D, Zhu M, Grogg K, Gerard S, Reinhardt J, Ribeiro G, Rashid A, Winkler T, Vidal Melo M. Mechanical ventilation guided by driving pressure optimizes local pulmonary biomechanics in an ovine model. Science Translational Medicine 2024, 16: eado1097. PMID: 39141699, DOI: 10.1126/scitranslmed.ado1097.Peer-Reviewed Original ResearchConceptsPositive end-expiratory pressureMechanical ventilationFour-dimensional computed tomographyParenchymal strainsVentilator-induced lung injuryAcute respiratory distress syndromeRespiratory system driving pressureManagement of mechanical ventilationPositive end-expiratory pressure valuesRespiratory distress syndromeTidal overdistensionEnd-expiratory pressureAssociated with mortalityPulmonary complicationsLung biomechanicsLung massDistress syndromeClinical outcomesLung injuryComputed tomographyClinical managementGeneral anesthesiaLung collapseDriving pressureLungRecruited atypical Ly6G+ macrophages license alveolar regeneration after lung injury
Ruscitti C, Abinet J, Maréchal P, Meunier M, de Meeûs C, Vanneste D, Janssen P, Dourcy M, Thiry M, Bureau F, Schneider C, Machiels B, Hidalgo A, Ginhoux F, Dewals B, Guiot J, Schleich F, Garigliany M, Bellahcène A, Radermecker C, Marichal T. Recruited atypical Ly6G+ macrophages license alveolar regeneration after lung injury. Science Immunology 2024, 9: eado1227-eado1227. PMID: 39093958, PMCID: PMC7616420, DOI: 10.1126/sciimmunol.ado1227.Peer-Reviewed Original ResearchConceptsLung injuryAlveolar regenerationGranulocyte-macrophage colony-stimulating factorColony-stimulating factorType 2 epithelial cellsAlveolar type 2 epithelial cellsPopulation of macrophagesModels of injuryImmune cellsSuspected pneumoniaA virusAlveolar damageEpithelial regenerationInterleukin-4Lung damageMacrophage subsetsReceptor signalingLungPerilesional areaRepair responseMacrophagesTherapeutic targetInjuryCellsAirborne pathogensSingle-cell RNA-seq analysis of cell-cell communications in human lung reveals a novel role of VEGF-D in acute lung injury
Yuan Y, Sharma L, Tang W, Raredon M, Ahangari F, Khoury J, Wu D, Niklason L, Kaminski N. Single-cell RNA-seq analysis of cell-cell communications in human lung reveals a novel role of VEGF-D in acute lung injury. Physiology 2024, 39: 1314. DOI: 10.1152/physiol.2024.39.s1.1314.Peer-Reviewed Original ResearchIdiopathic pulmonary fibrosisAcute lung injuryChronic obstructive pulmonary diseaseAcute respiratory distress syndromeAnalysis of cell-cell communicationVEGF-DMicrovascular nicheSingle-cell RNA-seqLung injury modelSingle-cell RNA-seq analysisLung injuryCell-cell communicationLigand-receptor pairsLPS-induced lung injury modelRNA-seqAdjacent cell typesPulmonary diseaseInjury modelHuman lung endothelial cellsBarrier functionImmune cell infiltrationTumor necrosis factor-aRespiratory distress syndromeLung vascular integrityGene expressionLung Epithelium Releases Growth Differentiation Factor 15 in Response to Pathogen-mediated Injury
Shah F, Bahudhanapati H, Jiang M, Tabary M, van der Geest R, Tolman N, Kochin M, Xiong Z, Al-Yousif N, Sayed K, Benos P, Raffensperger K, Evankovich J, Neal M, Snyder M, Eickelberg O, Ray P, Dela Cruz C, Bon J, McVerry B, Straub A, Jurczak M, Suber T, Zhang Y, Chen K, Kitsios G, Lee J, Alder J, Bain W. Lung Epithelium Releases Growth Differentiation Factor 15 in Response to Pathogen-mediated Injury. American Journal Of Respiratory Cell And Molecular Biology 2024, 70: 379-391. PMID: 38301257, PMCID: PMC11109583, DOI: 10.1165/rcmb.2023-0429oc.Peer-Reviewed Original ResearchConceptsLung injuryPlasma levelsLung epitheliumGDF15 levelsAssociated with plasma levelsAcute respiratory distress syndromeGrowth differentiation factor 15Acute respiratory failureRespiratory distress syndromeWild-type miceLung cytokine levelsHuman lung epitheliumAcute lung injuryDifferentiation factor 15Levels of GDF15Critically ill humansPrognostic of mortalitySARS-CoV-2 infectionCirculating GDF15 levelsRespiratory tract levelRespiratory failureDistress syndromeCytokine profileStress cytokinesCytokine levelsMAP kinase phosphatase-1 inhibition of p38α within lung myofibroblasts is essential for spontaneous fibrosis resolution
Fortier S, Walker N, Penke L, Baas J, Shen Q, Speth J, Huang S, Zemans R, Bennett A, Peters-Golden M. MAP kinase phosphatase-1 inhibition of p38α within lung myofibroblasts is essential for spontaneous fibrosis resolution. Journal Of Clinical Investigation 2024, 134: e172826. PMID: 38512415, PMCID: PMC11093610, DOI: 10.1172/jci172826.Peer-Reviewed Original ResearchConceptsMAPK phosphatase 1Fibrosis resolutionPulmonary fibrosisSpontaneous resolutionLung fibrosisBleomycin-induced lung fibrosisLung fibroblastsProgressive pulmonary fibrosisFibroblast-specific deletionExperimental lung fibrosisCells to apoptosisLung injuryRegulation of MAPK activityApoptosis-resistant myofibroblastsTransgenic miceResident fibroblastsTissue injuryFibrosisLung myofibroblastsLoss-of-function studiesGain- and loss-of-function studiesLungVX-702MyofibroblastsMAPK activationDedifferentiated early postnatal lung myofibroblasts redifferentiate in adult disease
Chandran R, Adams T, Kabir I, Gallardo-Vara E, Kaminski N, Gomperts B, Greif D. Dedifferentiated early postnatal lung myofibroblasts redifferentiate in adult disease. Frontiers In Cell And Developmental Biology 2024, 12: 1335061. PMID: 38572485, PMCID: PMC10987733, DOI: 10.3389/fcell.2024.1335061.Peer-Reviewed Original ResearchRNA sequencing analysisSMA+ myofibroblastsGene expression profilesLung myofibroblastsAdult lungSequence analysisResponse to lung injurySingle cell RNA sequencing analysisTissue remodeling genesSmooth muscle cell markersLung to hypoxiaExpression profilesRemodeling genesMuscle cell markersResponse to injuryCell typesSMA cellsLineage tracingLung injuryCell markersLineagesGenesAdult diseaseDrug bleomycinLung surface areaIntraoperative mechanical power and postoperative pulmonary complications in low-risk surgical patients: a prospective observational cohort study
El-Khatib M, Zeeni C, Shebbo F, Karam C, Safi B, Toukhtarian A, Nafeh N, Mkhayel S, Shadid C, Chalhoub S, Beresian J. Intraoperative mechanical power and postoperative pulmonary complications in low-risk surgical patients: a prospective observational cohort study. BMC Anesthesiology 2024, 24: 82. PMID: 38413871, PMCID: PMC10898029, DOI: 10.1186/s12871-024-02449-1.Peer-Reviewed Original ResearchConceptsPostoperative pulmonary complicationsLow-risk surgical patientsPulmonary complicationsSurgical patientsMechanical ventilationRisk of postoperative pulmonary complicationsGeneral anesthesiaVentilator-induced lung injuryIntraoperative mechanical ventilationAverage body mass indexPeak inspiratory pressureBody mass indexMultivariate regression analysisIntraoperative MPCritical care patientsHospital stayLung injuryInspiratory pressureMass indexElective surgeryIncreased riskTidal volumePatientsDays post-dischargeComplicationsAnti-inflammatory roles of type I interferon signaling in the lung
Feng J, Liu Y, Kim J, Ahangari F, Kaminski N, Bain W, Jie Z, Dela Cruz C, Sharma L. Anti-inflammatory roles of type I interferon signaling in the lung. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2024, 326: l551-l561. PMID: 38375579, DOI: 10.1152/ajplung.00353.2023.Peer-Reviewed Original ResearchType I interferon signalingIfnar1-/- miceI interferon signalingInflammatory cell responseInflammatory responseIfnar1-/-Bleomycin injuryCell responsesWild-type miceBroncho-alveolar lavageElevated inflammatory responsePersistent inflammatory responseChemotherapeutic agent bleomycinAnti-inflammatory roleClinically relevant stimuliAnti-inflammatory mechanismsMyeloid cellsPersistent inflammationLung injuryFibrotic remodelingBacterial clearanceRIG-I signalingNOD-like receptor signalingLung tissueReceptor signalingRecapitulation of human pathophysiology and identification of forensic biomarkers in a translational model of chlorine inhalation injury
Achanta S, Gentile M, Albert C, Schulte K, Pantazides B, Crow B, Quiñones-González J, Perez J, Ford D, Patel R, Blake T, Gunn M, Jordt S. Recapitulation of human pathophysiology and identification of forensic biomarkers in a translational model of chlorine inhalation injury. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2024, 326: l482-l495. PMID: 38318664, PMCID: PMC11281795, DOI: 10.1152/ajplung.00162.2023.Peer-Reviewed Original ResearchAcute lung injuryBronchoalveolar lavage fluidChlorine gasChlorinated fatty acidsDecreased dynamic lung complianceHuman acute lung injuryPeak inspiratory pressureIncreased airway resistanceMedical countermeasuresControlled mechanical ventilationForensic biomarkersDynamic lung complianceFormation of microthrombiProtein adductsAir-exposed groupNeutrophilic alveolitisTesting medical countermeasuresVascular leakageNeutrophil countPulmonary edemaHistopathological featuresPotential medical countermeasuresForensic analysisInspiratory pressureLung injuryHypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets
Fritz K, Sanidas G, Cardenas R, Ghaemmaghami J, Byrd C, Simonti G, Valenzuela A, Valencia I, Delivoria-Papadopoulos M, Gallo V, Koutroulis I, Dean T, Kratimenos P. Hypercapnia Causes Injury of the Cerebral Cortex and Cognitive Deficits in Newborn Piglets. ENeuro 2024, 11: eneuro.0268-23.2023. PMID: 38233145, PMCID: PMC10913040, DOI: 10.1523/eneuro.0268-23.2023.Peer-Reviewed Original ResearchConceptsNeonatal intensive care unitIntensive care unitCare unitCortical neuronsCerebral cortexCritically ill newbornsEnergy failureSevere lung injuryCortical neuronal injuryLong-term suppressionImpaired neurobehaviorExposure to hypercapniaNeurodevelopmental outcomesIll newbornsLung injuryLipid peroxidationElectroencephalogram frequencyNeuronal injuryPersistent dysregulationDeoxyribonucleic acid fragmentationAssociated with changesNewbornsEffect of HCHypercapniaProapoptotic signaling
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