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 recoveryLung 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 levelsIntranasal neomycin evokes broad-spectrum antiviral immunity in the upper respiratory tract
Mao T, Kim J, Peña-Hernández M, Valle G, Moriyama M, Luyten S, Ott I, Gomez-Calvo M, Gehlhausen J, Baker E, Israelow B, Slade M, Sharma L, Liu W, Ryu C, Korde A, Lee C, Monteiro V, Lucas C, Dong H, Yang Y, Initiative Y, Gopinath S, Wilen C, Palm N, Dela Cruz C, Iwasaki A, Vogels C, Hahn A, Chen N, Breban M, Koch T, Chaguza C, Tikhonova I, Castaldi C, Mane S, De Kumar B, Ferguson D, Kerantzas N, Peaper D, Landry M, Schulz W, Grubaugh N. Intranasal neomycin evokes broad-spectrum antiviral immunity in the upper respiratory tract. Proceedings Of The National Academy Of Sciences Of The United States Of America 2024, 121: e2319566121. PMID: 38648490, PMCID: PMC11067057, DOI: 10.1073/pnas.2319566121.Peer-Reviewed Original ResearchConceptsInterferon-stimulated genesRespiratory infectionsStrains of influenza A virusTreatment of respiratory viral infectionsRespiratory virus infectionsInfluenza A virusMouse model of COVID-19Respiratory viral infectionsNeomycin treatmentExpression of interferon-stimulated genesUpper respiratory infectionInterferon-stimulated gene expressionLower respiratory infectionsBroad spectrum of diseasesAdministration of neomycinRespiratory viral diseasesDisease to patientsUpper respiratory tractIntranasal deliveryCongenic miceIntranasal applicationNasal mucosaSevere acute respiratory syndrome coronavirus 2Acute respiratory syndrome coronavirus 2A virus
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
2011
Role of Chitin and Chitinase/Chitinase-Like Proteins in Inflammation, Tissue Remodeling, and Injury
Lee CG, Da Silva CA, Dela Cruz CS, Ahangari F, Ma B, Kang MJ, He CH, Takyar S, Elias JA. Role of Chitin and Chitinase/Chitinase-Like Proteins in Inflammation, Tissue Remodeling, and Injury. Annual Review Of Physiology 2011, 73: 479-501. PMID: 21054166, PMCID: PMC3864643, DOI: 10.1146/annurev-physiol-012110-142250.Peer-Reviewed Original ResearchConceptsBRP-39/YKLAdaptive Th2 immunityTissue remodelingChitinase-like proteinsAlternative macrophage activationTh2 inflammationInnate inflammationLung injuryTh2 immunityAcidic mammalian chitinaseAncient gene familyIL-13YKL-40Tissue injuryNumber of chitinasesEffector functionsMacrophage activationFamily of chitinasesInflammationDisease severityInjuryRole of chitinMammalian chitinaseGene familyEndogenous chitinRIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism
Ma B, Dela Cruz CS, Hartl D, Kang MJ, Takyar S, Homer RJ, Lee CG, Elias JA. RIG-like Helicase Innate Immunity Inhibits Vascular Endothelial Growth Factor Tissue Responses via a Type I IFN–dependent Mechanism. American Journal Of Respiratory And Critical Care Medicine 2011, 183: 1322-1335. PMID: 21278304, PMCID: PMC3114061, DOI: 10.1164/rccm.201008-1276oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDEAD Box Protein 58DEAD-box RNA HelicasesDisease Models, AnimalEdemaFocal Adhesion Protein-Tyrosine KinasesImmunity, InnateInflammationInterferon Type IMiceMice, TransgenicMitogen-Activated Protein KinasesNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasePoly I-CPulmonary Disease, Chronic ObstructiveToll-Like Receptor 3Vascular Endothelial Growth Factor AConceptsVascular endothelial growth factorType 2 inflammationChronic obstructive pulmonary disease exacerbationsObstructive pulmonary disease exacerbationsChronic obstructive pulmonary diseaseViral pathogen-associated molecular patternsEndothelial nitric oxide synthaseRIG-like helicasePulmonary disease exacerbationsObstructive pulmonary diseasePathogenesis of asthmaRespiratory syncytial virusNormal pulmonary physiologyNitric oxide synthaseAntiviral innate immunityPathogen-associated molecular patternsReceptor-dependent pathwayTissue responseEndothelial growth factorVEGF receptor 1Ability of VEGFDisease exacerbationPulmonary diseaseRespiratory virusesControl mice
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
2008
Cigarette smoke selectively enhances viral PAMP– and virus-induced pulmonary innate immune and remodeling responses in mice
Kang MJ, Lee CG, Lee JY, Dela Cruz CS, Chen ZJ, Enelow R, Elias JA. Cigarette smoke selectively enhances viral PAMP– and virus-induced pulmonary innate immune and remodeling responses in mice. Journal Of Clinical Investigation 2008, 118: 2771-2784. PMID: 18654661, PMCID: PMC2483678, DOI: 10.1172/jci32709.Peer-Reviewed Original ResearchConceptsChronic obstructive pulmonary diseaseMitochondrial antiviral signaling proteinCigarette smokeDisease exacerbationIFN-gammaInnate immunityViral PAMPsEffects of CSIL-12/ILSevere disease exacerbationsObstructive pulmonary diseaseEffects of influenzaType I IFNAirway fibrosisAirway inflammationLung functionPulmonary diseasePulmonary inflammationIL-18IL-18RalphaI IFNMurine lungViral infectionInflammationRNA-dependent protein kinase
2002
Breakdown of CTL Tolerance to Self HLA-B*2705 Induced by Exposure to Chlamydia trachomatis
Popov I, Dela Cruz CS, Barber BH, Chiu B, Inman RD. Breakdown of CTL Tolerance to Self HLA-B*2705 Induced by Exposure to Chlamydia trachomatis. The Journal Of Immunology 2002, 169: 4033-4038. PMID: 12244206, DOI: 10.4049/jimmunol.169.7.4033.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, Genetically ModifiedAutoantigensCells, CulturedChlamydia trachomatisCoculture TechniquesCytotoxicity, ImmunologicEpitopes, T-LymphocyteHLA-B AntigensHLA-B27 AntigenHumansL CellsLymphocyte ActivationLymphocyte Culture Test, MixedMiceRatsRats, Inbred LewSelf ToleranceT-Lymphocytes, CytotoxicTransfectionConceptsB27-transgenic ratsSuch immunized animalsGeneration of CTLMHC class IArthritogenic pathogensSelf-HLASeronegative arthritisCTL toleranceHLA-B27Arthritogenic peptidesCTL recognitionImmunized animalsRestriction elementsTransgenic ratsChlamydia trachomatisB27Disease pathogenesisSplenocytesClass IStrong associationCTLIntracellular bacteriaImmunizationChlamydiaRats