2021
Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity
Bui LT, Winters NI, Chung MI, Joseph C, Gutierrez AJ, Habermann AC, Adams TS, Schupp JC, Poli S, Peter LM, Taylor CJ, Blackburn JB, Richmond BW, Nicholson AG, Rassl D, Wallace WA, Rosas IO, Jenkins RG, Kaminski N, Kropski JA, Banovich NE. Chronic lung diseases are associated with gene expression programs favoring SARS-CoV-2 entry and severity. Nature Communications 2021, 12: 4314. PMID: 34262047, PMCID: PMC8280215, DOI: 10.1038/s41467-021-24467-0.Peer-Reviewed Original ResearchConceptsChronic lung diseaseLung diseaseImmune responseSARS-CoV-2 entry factorsSevere coronavirus disease-19SARS-CoV-2 infectionWorse COVID-19 outcomesSARS-CoV-2 entryAdaptive immune responsesCoronavirus disease-19COVID-19 outcomesInnate immune responseInflammatory gene expression programSimilar cellular distributionPoor outcomePeripheral lungViral exposureDisease-19Inflammatory microenvironmentEntry factorsLung epitheliumLung cellsViral replicationAT2 cellsBasal differences
2020
Mitochondrial antiviral signaling protein is crucial for the development of pulmonary fibrosis
Kim SH, Lee JY, Yoon CM, Shin HJ, Lee SW, Rosas I, Herzog E, Dela Cruz C, Kaminski N, Kang MJ. Mitochondrial antiviral signaling protein is crucial for the development of pulmonary fibrosis. European Respiratory Journal 2020, 57: 2000652. PMID: 33093124, PMCID: PMC8559259, DOI: 10.1183/13993003.00652-2020.Peer-Reviewed Original ResearchConceptsDamage-associated molecular patternsIdiopathic pulmonary fibrosisPulmonary fibrosisMAVS aggregationMultiple damage-associated molecular patternsExperimental pulmonary fibrosisMitochondrial antiviral signaling proteinInnate immune responseIPF patientsMAVS signalingIPF treatmentBleomycin injuryLung fibrosisTherapeutic effectImmune responseTherapeutic strategiesMAVS expressionFibrosisDanger signalsCritical mediatorMolecular patternsABT-263LungInjuryBH3 mimetics
2018
BPIFA1 regulates lung neutrophil recruitment and interferon signaling during acute inflammation
Britto CJ, Niu N, Khanal S, Huleihel L, Herazo-Maya J, Thompson A, Sauler M, Slade MD, Sharma L, Dela Cruz CS, Kaminski N, Cohn LE. BPIFA1 regulates lung neutrophil recruitment and interferon signaling during acute inflammation. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2018, 316: l321-l333. PMID: 30461288, PMCID: PMC6397348, DOI: 10.1152/ajplung.00056.2018.Peer-Reviewed Original ResearchConceptsLung inflammationAcute inflammationC motif chemokine ligand 10Lung neutrophil recruitmentRegulation of CXCL10Acute lung inflammationBronchoalveolar lavage concentrationsChemokine ligand 10Innate immune responseIFN regulatory factorIntranasal LPSLavage concentrationsLung recruitmentNeutrophil recruitmentWT miceImmune effectsLung diseasePMN recruitmentInflammatory responseLPS treatmentLung tissueInflammatory signalsImmune responseImmunomodulatory propertiesInflammation
2015
Suppression of NLRX1 in chronic obstructive pulmonary disease
Kang MJ, Yoon CM, Kim BH, Lee CM, Zhou Y, Sauler M, Homer R, Dhamija A, Boffa D, West AP, Shadel GS, Ting JP, Tedrow JR, Kaminski N, Kim WJ, Lee CG, Oh YM, Elias JA. Suppression of NLRX1 in chronic obstructive pulmonary disease. Journal Of Clinical Investigation 2015, 125: 2458-2462. PMID: 25938787, PMCID: PMC4497738, DOI: 10.1172/jci71747.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseObstructive pulmonary diseaseCigarette smokeAlveolar destructionPulmonary diseaseHuman chronic obstructive pulmonary diseaseExpression of NLRX1Innate immune pathwaysInnate immune responseQuality of lifeCOPD patientsPulmonary functionSubsequent inflammationImmune responseInflammasome activationMurine modelIndependent cohortImmune pathwaysInflammationDisease severityInflammasome responseImportant mediatorCell apoptosisNLRX1Tissue effects
2009
Systemic Inhibition of NF-κB Activation Protects from Silicosis
Di Giuseppe M, Gambelli F, Hoyle GW, Lungarella G, Studer SM, Richards T, Yousem S, McCurry K, Dauber J, Kaminski N, Leikauf G, Ortiz LA. Systemic Inhibition of NF-κB Activation Protects from Silicosis. PLOS ONE 2009, 4: e5689. PMID: 19479048, PMCID: PMC2682759, DOI: 10.1371/journal.pone.0005689.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCytokinesEpithelial CellsFemaleGene Expression RegulationGenes, DominantHumansI-kappa B ProteinsLungLung TransplantationMacrophagesMaleMiceMice, Inbred C57BLMiddle AgedNF-kappa BNF-KappaB Inhibitor alphaNitrilesPrognosisRNA, MessengerSilicon DioxideSilicosisSulfonesTumor Necrosis Factor-alphaConceptsNF-kappaB activationLung transplantationSystemic inhibitionLung injuryCollagen depositionLung transplant databaseIdiopathic pulmonary fibrosisComplex lung diseaseNecrosis factor alphaPathogenesis of silicosisIkappaB-alpha phosphorylationInnate immune responsePotential therapeutic strategyNF-kappaB inhibitionMouse experimental modelIPF patientsLung graftsGraft rejectionOverall survivalSurvival benefitTransplant databasePulmonary fibrosisPoor outcomeInflammatory cellsLung disease