2024
Context‐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 recoveryLongitudinal multicompartment characterization of host-microbiota interactions in patients with acute respiratory failure
Kitsios G, Sayed K, Fitch A, Yang H, Britton N, Shah F, Bain W, Evankovich J, Qin S, Wang X, Li K, Patel A, Zhang Y, Radder J, Dela Cruz C, Okin D, Huang C, Van Tyne D, Benos P, Methé B, Lai P, Morris A, McVerry B. Longitudinal multicompartment characterization of host-microbiota interactions in patients with acute respiratory failure. Nature Communications 2024, 15: 4708. PMID: 38830853, PMCID: PMC11148165, DOI: 10.1038/s41467-024-48819-8.Peer-Reviewed Original ResearchConceptsAcute respiratory failureRespiratory failureCohort of COVID-19 patientsLung microbiotaMechanically ventilated patientsChronic obstructive pulmonary diseaseIllumina amplicon sequencingDNA sequencing technologiesHost-microbiota interactionsObstructive pulmonary diseaseCOVID-19 patientsAssociated with specific patternsAntibiotic exposureClinical factorsNanopore metagenomicsPredicting survivalPrecision medicine interventionsPrognostic biomarkerSequencing technologiesAmplicon sequencingPulmonary diseaseGut microbiotaCritical illnessMicrobial diversityHuman microbiomeLung 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 levels
2015
Regulation of Retinoic Acid Receptor Beta by Interleukin-15 in the Lung during Cigarette Smoking and Influenza Virus Infection
Wang J, Liu W, Marion C, Singh R, Andrews N, Lee CG, Elias JA, Dela Cruz CS. Regulation of Retinoic Acid Receptor Beta by Interleukin-15 in the Lung during Cigarette Smoking and Influenza Virus Infection. American Journal Of Respiratory Cell And Molecular Biology 2015, 53: 822-833. PMID: 25923039, PMCID: PMC4742936, DOI: 10.1165/rcmb.2014-0448oc.Peer-Reviewed Original ResearchConceptsInfluenza virus infectionCS exposureVirus infectionIL-15WT miceIL-15 knockout miceIL-15 receptor αIL-15 transgenic miceLong-term CS exposureChronic obstructive pulmonary diseaseIL-15tg miceLung interstitial macrophagesCigarette smoke exposureVirus-induced exacerbationsObstructive pulmonary diseaseAntiviral immune responseWild-type miceRetinoic acid receptor betaRA receptor βAcid receptor betaLung injuryLung functionPulmonary diseaseRARβ expressionSmoke exposure
2012
Chitinase 3-like-1 Promotes Streptococcus pneumoniae Killing and Augments Host Tolerance to Lung Antibacterial Responses
Dela Cruz CS, Liu W, He CH, Jacoby A, Gornitzky A, Ma B, Flavell R, Lee CG, Elias JA. Chitinase 3-like-1 Promotes Streptococcus pneumoniae Killing and Augments Host Tolerance to Lung Antibacterial Responses. Cell Host & Microbe 2012, 12: 34-46. PMID: 22817986, PMCID: PMC3613130, DOI: 10.1016/j.chom.2012.05.017.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsCarrier ProteinsCaspase 1Cell DeathChitinase-3-Like Protein 1CytokinesGlycoproteinsHost-Pathogen InteractionsInflammasomesLungMacrophagesMiceMice, Mutant StrainsNLR Family, Pyrin Domain-Containing 3 ProteinPhagocytosisPneumococcal InfectionsPneumonia, PneumococcalReceptors, Purinergic P2X7Streptococcus pneumoniaeConceptsHost toleranceAntibacterial responseChitinase-like proteinsEvolutionary timeHost antibacterial responsesATP accumulationChitinase 3Bacterial clearanceCentral roleMacrophage pyroptosisToleranceBacterial disseminationInflammasome activationStreptococcus pneumoniaeBacterial killingType 17 cytokinesThymic stromal lymphopoietinCHI3L1SpeciesProteinBacteriaLung injuryHostRolePyroptosis
2010
Transgenic modelling of cytokine polarization in the lung
Dela Cruz CS, Kang M, Cho W, Lee CG. Transgenic modelling of cytokine polarization in the lung. Immunology 2010, 132: 9-17. PMID: 21091906, PMCID: PMC3015070, DOI: 10.1111/j.1365-2567.2010.03376.x.Peer-Reviewed Original ResearchConceptsCytokine polarizationT helper type 17 cytokinesT helper type 2T helper type 1Type 1Type 17 cytokinesHelper type 2Type 2 cytokinesHelper type 1Human lung diseasesVariety of cytokinesCytokine milieuPulmonary inflammationEnvironmental allergensLung diseaseTissue phenotypeInjury modelT-betCommon siteCertain cytokinesEffector functionsTransgenic miceIndividual cytokinesPathophysiological consequencesType 2Role of Breast Regression Protein–39 in the Pathogenesis of Cigarette Smoke–Induced Inflammation and Emphysema
Matsuura H, Hartl D, Kang MJ, Dela Cruz CS, Koller B, Chupp GL, Homer RJ, Zhou Y, Cho WK, Elias JA, Lee CG. Role of Breast Regression Protein–39 in the Pathogenesis of Cigarette Smoke–Induced Inflammation and Emphysema. American Journal Of Respiratory Cell And Molecular Biology 2010, 44: 777-786. PMID: 20656949, PMCID: PMC3135840, DOI: 10.1165/rcmb.2010-0081oc.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseBRP-39/YKLBreast regression protein 39YKL-40BRP-39Alveolar destructionCigarette smokeChitinase-like protein YKL-40Emphysematous alveolar destructionLungs of CSObstructive pulmonary diseaseProtein YKL-40Excessive inflammatory responseAirway epithelial cellsAlveolar type II cellsNull mutant miceProtein 39Epithelial cell apoptosisType II cellsCurrent smokersPulmonary diseaseBronchoalveolar lavageTissue inflammationEmphysematous destructionSerum concentrations