2024
A common polymorphism in the Intelectin-1 gene influences mucus plugging in severe asthma
Everman J, Sajuthi S, Liegeois M, Jackson N, Collet E, Peters M, Chioccioli M, Moore C, Patel B, Dyjack N, Powell R, Rios C, Montgomery M, Eng C, Elhawary J, Mak A, Hu D, Huntsman S, Salazar S, Feriani L, Fairbanks-Mahnke A, Zinnen G, Michel C, Gomez J, Zhang X, Medina V, Chu H, Cicuta P, Gordon E, Zeitlin P, Ortega V, Reisdorph N, Dunican E, Tang M, Elicker B, Henry T, Bleecker E, Castro M, Erzurum S, Israel E, Levy B, Mauger D, Meyers D, Sumino K, Gierada D, Hastie A, Moore W, Denlinger L, Jarjour N, Schiebler M, Wenzel S, Woodruff P, Rodriguez-Santana J, Pearson C, Burchard E, Fahy J, Seibold M. A common polymorphism in the Intelectin-1 gene influences mucus plugging in severe asthma. Nature Communications 2024, 15: 3900. PMID: 38724552, PMCID: PMC11082194, DOI: 10.1038/s41467-024-48034-5.Peer-Reviewed Original ResearchConceptsAirway epithelial cellsIntelectin-1Mucus pluggingGene expressionAirways of severe asthmaticsEpithelial cellsHuman airway epithelial cellsAirway epithelial brushingsMucus secretory cellsT2-high asthmaFormation of mucus plugsAssociated with protectionC-terminusGenetic variantsAirway mucus pluggingMolecular roleSecretory cellsSecreted componentsEpithelial brushingsT2-lowIL-13Mucus obstructionTarget pathwaysSevere asthmaticsClinical significance
2022
Mucus sialylation determines intestinal host-commensal homeostasis
Yao Y, Kim G, Shafer S, Chen Z, Kubo S, Ji Y, Luo J, Yang W, Perner SP, Kanellopoulou C, Park AY, Jiang P, Li J, Baris S, Aydiner EK, Ertem D, Mulder DJ, Warner N, Griffiths AM, Topf-Olivestone C, Kori M, Werner L, Ouahed J, Field M, Liu C, Schwarz B, Bosio CM, Ganesan S, Song J, Urlaub H, Oellerich T, Malaker SA, Zheng L, Bertozzi CR, Zhang Y, Matthews H, Montgomery W, Shih HY, Jiang J, Jones M, Baras A, Shuldiner A, Gonzaga-Jauregui C, Snapper SB, Muise AM, Shouval DS, Ozen A, Pan KT, Wu C, Lenardo MJ. Mucus sialylation determines intestinal host-commensal homeostasis. Cell 2022, 185: 1172-1188.e28. PMID: 35303419, PMCID: PMC9088855, DOI: 10.1016/j.cell.2022.02.013.Peer-Reviewed Original ResearchConceptsInflammatory bowel diseaseMicrobial pathogen-associated molecular patternsPathogen-associated molecular patternsMicrobial symbiosisRegulatory networksIntestinal mucusGlycoproteomic profilingMolecular patternsTerminal sialylationMucus proteinsProteolytic degradationBiochemical analysisBacterial invasionBowel diseaseIntestinal inflammationMucus integrityMutationsSialylationST6GALNAC1Barrier integrityGoblet cellsMucus barrierFirst lineSymbiosisCommensalism
2020
Single-Cell and Population Transcriptomics Reveal Pan-epithelial Remodeling in Type 2-High Asthma
Jackson ND, Everman JL, Chioccioli M, Feriani L, Goldfarbmuren KC, Sajuthi SP, Rios CL, Powell R, Armstrong M, Gomez J, Michel C, Eng C, Oh SS, Rodriguez-Santana J, Cicuta P, Reisdorph N, Burchard EG, Seibold MA. Single-Cell and Population Transcriptomics Reveal Pan-epithelial Remodeling in Type 2-High Asthma. Cell Reports 2020, 32: 107872. PMID: 32640237, PMCID: PMC8046336, DOI: 10.1016/j.celrep.2020.107872.Peer-Reviewed Original ResearchConceptsIL-13Single-cell RNA sequencingHuman airway epithelial cell culturesCell typesIL-13 effectsAirway epithelial cell culturesNasal airway epitheliumCandidate therapeutic targetTranscriptional statesAsthmatic childrenAsthma endotypesRNA sequencingMucus obstructionAirway epitheliumSecretory programMucin productionNormal epithelial functionTherapeutic targetEpithelial cell culturesCellular remodelingER stressCell deathEpithelial functionMetaplastic stateSecretory cells
2019
Escalating Mucus Inhibition to the Top of Our Priorities
Britto CJ, Cohn L. Escalating Mucus Inhibition to the Top of Our Priorities. American Journal Of Respiratory Cell And Molecular Biology 2019, 61: 275-276. PMID: 31063695, PMCID: PMC6839933, DOI: 10.1165/rcmb.2019-0143ed.Commentaries, Editorials and Letters
2015
Quantifying hyperoxia-mediated damage to mammalian respiratory cilia-driven fluid flow using particle tracking velocimetry optical coherence tomography
Gamm UA, Huang BK, Syed M, Zhang X, Bhandari V, Choma MA. Quantifying hyperoxia-mediated damage to mammalian respiratory cilia-driven fluid flow using particle tracking velocimetry optical coherence tomography. Journal Of Biomedical Optics 2015, 20: 080505-080505. PMID: 26308164, PMCID: PMC4874052, DOI: 10.1117/1.jbo.20.8.080505.Peer-Reviewed Original ResearchConceptsOptical coherence tomographyMouse tracheaCoherence tomographyDrug-mediated modulationIntensive care unitRisk-benefit profileRespiratory failureCare unitOxygen supplementationRespiratory mucosaRespiratory epitheliumIndispensable treatmentImpaired capacityClinical useHyperoxiaTracheaFlow quantificationTomographyTreatmentDamagePatientsMucosaSupplementationEpitheliumHighly compacted biodegradable DNA nanoparticles capable of overcoming the mucus barrier for inhaled lung gene therapy
Mastorakos P, da Silva A, Chisholm J, Song E, Choi W, Boyle M, Morales M, Hanes J, Suk J. Highly compacted biodegradable DNA nanoparticles capable of overcoming the mucus barrier for inhaled lung gene therapy. Proceedings Of The National Academy Of Sciences Of The United States Of America 2015, 112: 8720-8725. PMID: 26124127, PMCID: PMC4507234, DOI: 10.1073/pnas.1502281112.Peer-Reviewed Original ResearchConceptsHigh-level transgene expressionGene delivery systemsDNA nanoparticlesTransgene expressionNanoparticle-based gene delivery systemGene therapyDelivery systemLung gene therapyRobust transgene expressionTherapeutic genesTransfection efficiencyColloidal stabilityNanoparticlesBiological barriersTunable platformPhysiological fluidsBiodegradable polymersDense coronaConventional therapeuticsMucus barrierPolyethylene glycolMucus gel layerTreatment of diseasesSignificant hurdlePBAE
2014
Regulation of Nasal Airway Homeostasis and Inflammation in Mice by SHP-1 and Th2/Th1 Signaling Pathways
Cho SH, Oh SY, Lane AP, Lee J, Oh MH, Lee S, Zheng T, Zhu Z. Regulation of Nasal Airway Homeostasis and Inflammation in Mice by SHP-1 and Th2/Th1 Signaling Pathways. PLOS ONE 2014, 9: e103685. PMID: 25090641, PMCID: PMC4121172, DOI: 10.1371/journal.pone.0103685.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChemokinesEosinophiliaGelatinHomeostasisInflammationInterferon-gammaMatrix Metalloproteinase 2Matrix Metalloproteinase 9MetaplasiaMice, Inbred C57BLMice, Mutant StrainsMucusNasal Lavage FluidNasal MucosaProtein Tyrosine Phosphatase, Non-Receptor Type 6RhinitisSignal TransductionTh1 CellsTh2 CellsConceptsMatrix metalloproteinasesNasal inflammationAllergic rhinitisTh1 cytokinesInflammatory cellsTh2 cytokinesNasal airwayChronic inflammatory diseaseExpression of cytokinesTh2-skewed inflammationIFN-γ geneMucus metaplasiaTh1 paradigmAirway homeostasisInflammatory mediatorsTh2 lymphocytesImmune homeostasisInflammatory diseasesViable motheaten miceInflammationTransepithelial migrationCytokinesMev miceClearance mechanismsTh2NLRP6 Inflammasome Orchestrates the Colonic Host-Microbial Interface by Regulating Goblet Cell Mucus Secretion
Wlodarska M, Thaiss CA, Nowarski R, Henao-Mejia J, Zhang JP, Brown EM, Frankel G, Levy M, Katz MN, Philbrick WM, Elinav E, Finlay BB, Flavell RA. NLRP6 Inflammasome Orchestrates the Colonic Host-Microbial Interface by Regulating Goblet Cell Mucus Secretion. Cell 2014, 156: 1045-1059. PMID: 24581500, PMCID: PMC4017640, DOI: 10.1016/j.cell.2014.01.026.Peer-Reviewed Original ResearchConceptsRegulatory pathwaysGoblet cell mucus secretionHost-microbial mutualismHost-microbial interfaceNLRP6 inflammasomeMucus secretionGoblet cellsBiogeographical distributionProkaryotic cellsInnate immune playersNLRP6 deficiencyGranule exocytosisImmune regulatory pathwaysInflammasome-deficient miceColonic microbiota compositionLarge intestinal lumenCritical orchestratorsImmune playersPersistent infectionMucus productionCellsIntestinal lumenPathwayMucosal surfacesMicrobiota composition
2009
Advances in Mucous Cell Metaplasia
Curran DR, Cohn L. Advances in Mucous Cell Metaplasia. American Journal Of Respiratory Cell And Molecular Biology 2009, 42: 268-275. PMID: 19520914, PMCID: PMC2830403, DOI: 10.1165/rcmb.2009-0151tr.BooksConceptsMucous cell metaplasiaCell metaplasiaMucous metaplasiaChronic obstructive pulmonary diseaseChronic airway diseasesObstructive pulmonary diseaseExacerbation of asthmaChronic airwayAirway obstructionAirway diseaseMucus hypersecretionPulmonary diseaseMolecular mechanismsHarmful insultsIL-13MUC5AC expressionEpidermal growth factor receptor (EGFR) activationGoblet cell granulesGrowth factor receptor activationMucin productionMucus productionNew therapiesGoblet cellsFront-line protectionMetaplasiaMucus Rupture (Extrusion) and Duct Expansion/Expansive Growth are not Diagnostic of Minimal Invasion When Seen With Intraductal Papillary Mucinous Neoplasms
Stelow E, Pambuccian S, Bauer T, Moskaluk C, Klimstra D. Mucus Rupture (Extrusion) and Duct Expansion/Expansive Growth are not Diagnostic of Minimal Invasion When Seen With Intraductal Papillary Mucinous Neoplasms. The American Journal Of Surgical Pathology 2009, 33: 320-321. PMID: 18824892, DOI: 10.1097/pas.0b013e3181861bcd.Peer-Reviewed Original Research
2008
A Critical Role of SHP-1 in Regulation of Type 2 Inflammation in the Lung
Oh SY, Zheng T, Kim YK, Cohn L, Homer RJ, McKenzie AN, Zhu Z. A Critical Role of SHP-1 in Regulation of Type 2 Inflammation in the Lung. American Journal Of Respiratory Cell And Molecular Biology 2008, 40: 568-574. PMID: 18952567, PMCID: PMC2677436, DOI: 10.1165/rcmb.2008-0225oc.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBronchial HyperreactivityBronchoalveolar Lavage FluidCytokinesEpitheliumHypertrophyLungLymphocyte ActivationMetaplasiaMiceMice, Inbred C57BLMucin 5ACMucusPneumoniaProtein Tyrosine Phosphatase, Non-Receptor Type 6Pulmonary FibrosisSignal TransductionSTAT6 Transcription FactorTh2 CellsConceptsSHP-1Src homology 2 domain-containing protein tyrosine phosphataseProtein tyrosine phosphataseGene deletion approachIL-4/ILViable motheaten miceMev miceCritical roleTyrosine phosphataseKey genesNegative regulatorSignal transducerMolecular mechanismsCytokine receptorsMotheaten miceTranscription 6Critical moleculesDirect roleType 2 inflammationChronic inflammatory disordersHallmark of asthmaLung homeostasisPathwayGrowth factorAirway hyperresponsivenessEndogenous IL-11 Signaling Is Essential in Th2- and IL-13–Induced Inflammation and Mucus Production
Lee CG, Hartl D, Matsuura H, Dunlop FM, Scotney PD, Fabri LJ, Nash AD, Chen NY, Tang CY, Chen Q, Homer RJ, Baca M, Elias JA. Endogenous IL-11 Signaling Is Essential in Th2- and IL-13–Induced Inflammation and Mucus Production. American Journal Of Respiratory Cell And Molecular Biology 2008, 39: 739-746. PMID: 18617680, PMCID: PMC2586049, DOI: 10.1165/rcmb.2008-0053oc.Peer-Reviewed Original ResearchConceptsIL-13 productionMucus productionIL-11Th2 inflammationIL-11RalphaAerosol antigen challengeAirway mucus productionBronchoalveolar lavage (BAL) inflammationPulmonary Th2 responsesLevels of IgEIL-13 responsesEndogenous IL-11Null mutant miceBAL inflammationMucus metaplasiaEosinophilic inflammationTh2 responsesAntigen challengeIL-11 receptorWT miceTh2 cytokinesIntraperitoneal administrationInflammationMucus responseMurine lungIL-13 Receptor α2 Selectively Inhibits IL-13-Induced Responses in the Murine Lung
Zheng T, Liu W, Oh SY, Zhu Z, Hu B, Homer RJ, Cohn L, Grusby MJ, Elias JA. IL-13 Receptor α2 Selectively Inhibits IL-13-Induced Responses in the Murine Lung. The Journal Of Immunology 2008, 180: 522-529. PMID: 18097054, DOI: 10.4049/jimmunol.180.1.522.Peer-Reviewed Original ResearchConceptsIL-13Ralpha2Pulmonary inflammationIL-13Inflammatory responseMurine lungHigh-affinity IL-13 receptorsTransgenic IL-13IL-13 receptor α2Production of chemokinesEnhanced inflammatory responseIL-13 receptorMucus metaplasiaTh2 inflammationAirway remodelingSubepithelial fibrosisIL-4Receptor α2Critical cytokineIL-13Ralpha1IL-4RalphaDecoy receptorPhysiologic responsesInflammationTissue effectsReceptors
2007
Inhibition of NF-κB Activation Reduces the Tissue Effects of Transgenic IL-13
Chapoval SP, Al-Garawi A, Lora JM, Strickland I, Ma B, Lee PJ, Homer RJ, Ghosh S, Coyle AJ, Elias JA. Inhibition of NF-κB Activation Reduces the Tissue Effects of Transgenic IL-13. The Journal Of Immunology 2007, 179: 7030-7041. PMID: 17982094, DOI: 10.4049/jimmunol.179.10.7030.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsApoptosisCaspasesHeterocyclic Compounds, 3-RingI-kappa B KinaseInflammationInhibitor of Apoptosis ProteinsInterleukin-13MiceMice, Mutant StrainsMice, TransgenicMucusNF-kappa B p50 SubunitPeptidesPulmonary AlveoliPulmonary FibrosisPyridinesReceptors, Cell SurfaceRespiratory HypersensitivitySignal TransductionTh2 CellsConceptsTransgenic IL-13IL-13Alveolar remodelingIL-13 transgenic miceNF-kappaBMajor Th2 cytokinesExcessive mucus productionTissue effectsNF-κB activationNF-kappaB activationNF-kappaB activityNF-kappaB componentsAirway hyperresponsivenessTh2 cytokinesTissue inflammationPharmacologic approachesMucus productionIL-13Ralpha1Murine lungSmall molecule inhibitorsTissue alterationsNF-kappaB.MiceCell apoptosisDiminished levelsRecombinant basic fibroblast growth factor inhibits the airway hyperresponsiveness, mucus production, and lung inflammation induced by an allergen challenge
Jeon SG, Lee CG, Oh MH, Chun EY, Gho YS, Cho SH, Kim JH, Min KU, Kim YY, Kim YK, Elias JA. Recombinant basic fibroblast growth factor inhibits the airway hyperresponsiveness, mucus production, and lung inflammation induced by an allergen challenge. Journal Of Allergy And Clinical Immunology 2007, 119: 831-837. PMID: 17289133, DOI: 10.1016/j.jaci.2006.12.653.Peer-Reviewed Original ResearchConceptsAsthma mouse modelLung inflammationBasic fibroblast growth factorAsthma phenotypesMucus productionFibroblast growth factorAllergen challengeTg miceRecombinant FGF2Therapeutic effectMouse modelWild-type control miceGrowth factorDevelopment of AHRTGF-beta1 miceRegional lymph nodesWhole-body plethysmographyDevelopment of asthmaBronchoalveolar lavage cellularityRecombinant basic fibroblast growth factorFGF2-deficient micePeriodic acid-Schiff stainingFGF2 mRNA expressionRole of FGF2Acid-Schiff stainingPseudomonas aeruginosa chronic colonization in cystic fibrosis patients
Murray TS, Egan M, Kazmierczak BI. Pseudomonas aeruginosa chronic colonization in cystic fibrosis patients. Current Opinion In Pediatrics 2007, 19: 83-88. PMID: 17224667, DOI: 10.1097/mop.0b013e3280123a5d.Peer-Reviewed Original ResearchConceptsCystic fibrosis patientsChronic colonizationAcute infectionFibrosis patientsCystic fibrosisP. aeruginosaChronic pulmonary colonizationChronic pulmonary diseaseCystic fibrosis airwayHost immune systemMucoid P. aeruginosaP. aeruginosa behaviorCystic fibrosis lungPulmonary diseaseClinical benefitChronic infectionP. aeruginosa pathogenesisLeading causePulmonary colonizationNew therapiesImmune systemAggressive usePotential therapeuticsInfectionPatients
2006
Essential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung
Bhandari V, Choo-Wing R, Chapoval SP, Lee CG, Tang C, Kim YK, Ma B, Baluk P, Lin MI, McDonald DM, Homer RJ, Sessa WC, Elias JA. Essential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung. Proceedings Of The National Academy Of Sciences Of The United States Of America 2006, 103: 11021-11026. PMID: 16832062, PMCID: PMC1544167, DOI: 10.1073/pnas.0601057103.Peer-Reviewed Original ResearchConceptsInducible NOSNitric oxideEndothelial NOS inhibitorDendritic cell activationNO-dependent mechanismAirway hyperresponsivenessMucus metaplasiaLymphocyte accumulationPulmonary alterationsCell hyperplasiaNOS inhibitorNormal micePhysiologic responsesCell activationInflammationENOSVEGFMiceIndependent mechanismsTissue responseLatter responseLungAngiogenesisRemodelingNull mutation
2005
Malignant mesothelioma with a pronounced myxoid stroma: a clinical and pathological evaluation of 19 cases
Shia J, Qin J, Erlandson R, King R, Illei P, Nobrega J, Yao D, Klimstra D. Malignant mesothelioma with a pronounced myxoid stroma: a clinical and pathological evaluation of 19 cases. Virchows Archiv 2005, 447: 828-834. PMID: 16021506, DOI: 10.1007/s00428-005-0035-y.Peer-Reviewed Original ResearchConceptsMyxoid stromaEpithelioid mesotheliomaSurvival rateMedian survival rateTumor cell componentsSurface microvilliExtracellular amorphous materialAdjuvant radiationExtrapleural pneumonectomyHistological subtypesTumor volumeCytologic atypiaMalignant mesotheliomaPathological evaluationPleural mesotheliomaTumor cellsPathological analysisMyxoid materialMesothelial immunophenotypeMesotheliomaPathological featuresTumorAsbestos exposureInclusion criteriaPatients
2002
Cytokine Regulation of Mucus Production in a Model of Allergic Asthma
Cohn L, Whittaker L, Niu N, Homer RJ. Cytokine Regulation of Mucus Production in a Model of Allergic Asthma. Novartis Foundation Symposia 2002, 248: 201-220. PMID: 12568496, DOI: 10.1002/0470860790.ch13.BooksMeSH KeywordsAdministration, InhalationAnimalsAsthmaBronchoalveolar Lavage FluidCells, CulturedExocytosisGene Expression RegulationImmunizationInterferon-gammaInterferonsInterleukin-13Interleukin-13 Receptor alpha1 SubunitInterleukin-4Interleukin-5Interleukin-9Mast CellsMiceMice, TransgenicModels, AnimalMucinsMucusOvalbuminPeptide FragmentsPulmonary EosinophiliaRadiation ChimeraReceptors, Antigen, T-Cell, alpha-betaReceptors, InterleukinReceptors, Interleukin-13Receptors, Interleukin-4Respiratory SystemSignal TransductionTh1 CellsTh2 CellsConceptsAirway inflammationTh2 cellsMucus productionTh1 cellsT cell receptor transgenic CD4Airway inflammatory infiltrateDifferent lymphocyte subsetsBone marrow chimerasAbsence of interleukinAirway obstructionAllergic asthmaLymphocyte subsetsEosinophilic inflammationMucus hyperproductionInflammatory infiltrateClinical symptomsInflammatory cellsTh2 lymphocytesRecipient miceTh cellsTransgenic CD4Respiratory tractMast cellsCytokine regulationInflammationIL-13-Induced Chemokine Responses in the Lung: Role of CCR2 in the Pathogenesis of IL-13-Induced Inflammation and Remodeling
Zhu Z, Ma B, Zheng T, Homer RJ, Lee CG, Charo IF, Noble P, Elias JA. IL-13-Induced Chemokine Responses in the Lung: Role of CCR2 in the Pathogenesis of IL-13-Induced Inflammation and Remodeling. The Journal Of Immunology 2002, 168: 2953-2962. PMID: 11884467, DOI: 10.4049/jimmunol.168.6.2953.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBronchoalveolar Lavage FluidCells, CulturedChemokine CCL2Chemokines, CCEndopeptidasesHyaluronic AcidInflammationInterleukin-13LungLung ComplianceMetaplasiaMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMinkMucusPhenotypeProtease InhibitorsPulmonary AlveoliPulmonary FibrosisReceptors, CCR2Receptors, ChemokineRespiratory InsufficiencyRespiratory MucosaRNA, MessengerTotal Lung CapacityTransforming Growth Factor betaTransforming Growth Factor beta1ConceptsMonocyte chemotactic proteinTransgenic IL-13IL-13Potent stimulatorIL-13 transgenic miceIL-13-induced inflammationSecretory leukocyte proteinase inhibitorRole of CCR2Macrophage-derived chemokineActivation-regulated chemokineMacrophage inflammatory proteinHyaluronic acid accumulationPathogenesis of humanMucus metaplasiaCCR2 deficiencyRespiratory failureChemokine responsesPulmonary inflammationLung complianceMIP-2Lavage fluidMIP-1betaEotaxin-2MCP-1MIP-3alpha
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