Genta Ishikawa, MD, MPH
InstructorCards
About
Research
Publications
2025
Damage 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 DNA
2024
INTERACTIONS BETWEEN MITOCHONDRIAL DNA AND TOLL-LIKE RECEPTOR 9 MEDIATES PULMONARY FIBROSIS
LEE C, TRUJILLO G, REGUEIRO-REN A, LIU C, HU B, SUN Y, KHOURY J, KHOURY J, AHANGARI F, ISHIKAWA G, WALIA A, PIVARNIK T, YU S, WOO S, FIORINI V, MCGOVERN J, AL JUMAILY K, SUN H, PENG X, ANTIN-OZERKIS D, SAULER M, KAMINSKI N, HERZOG E. INTERACTIONS BETWEEN MITOCHONDRIAL DNA AND TOLL-LIKE RECEPTOR 9 MEDIATES PULMONARY FIBROSIS. CHEST Journal 2024, 166: a3384-a3386. DOI: 10.1016/j.chest.2024.06.2020.Peer-Reviewed Original ResearchToll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis.
Trujillo G, Regueiro-Ren A, Liu C, Hu B, Sun Y, Ahangari F, Fiorini V, Ishikawa G, Al Jumaily K, Khoury J, McGovern J, Lee C, Peng X, Pivarnik T, Sun H, Walia A, Woo S, Yu S, Antin-Ozerkis D, Sauler M, Kaminski N, Herzog E, Ryu C. Toll-like Receptor 9 Inhibition Mitigates Fibroproliferative Responses in Translational Models of Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2024, 211: 91-102. PMID: 39189851, PMCID: PMC11755360, DOI: 10.1164/rccm.202401-0065oc.Peer-Reviewed Original ResearchToll-like receptor 9Model of pulmonary fibrosisIdiopathic pulmonary fibrosisPulmonary fibrosisFibroproliferative responseLung diseaseIdiopathic pulmonary fibrosis cohortsExpression of toll-like receptor 9Toll-like receptor 9 activationTransplant-free survivalExpression of MCP-1Cohort of patientsSlow clinical progressionFibrotic lung diseaseAccelerated disease courseFatal lung diseaseIP-10Pharmacodynamic endpointsPreclinical modelsDisease courseClinical progressionPlasma mtDNAMCP-1Receptor 9Mouse modelSingle-Cell Profiling Reveals Immune Aberrations in Progressive Idiopathic Pulmonary Fibrosis.
Unterman A, Zhao A, Neumark N, Schupp J, Ahangari F, Cosme C, Sharma P, Flint J, Stein Y, Ryu C, Ishikawa G, Sumida T, Gomez J, Herazo-Maya J, Dela Cruz C, Herzog E, Kaminski N. Single-Cell Profiling Reveals Immune Aberrations in Progressive Idiopathic Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2024, 210: 484-496. PMID: 38717443, PMCID: PMC11351796, DOI: 10.1164/rccm.202306-0979oc.Peer-Reviewed Original ResearchStable idiopathic pulmonary fibrosisIdiopathic pulmonary fibrosisPeripheral blood mononuclear cellsProgressive idiopathic pulmonary fibrosisPeripheral immune systemT cellsPulmonary fibrosisCohort of IPF patientsAssociated with decreased survivalIdiopathic pulmonary fibrosis patientsPeripheral blood mononuclear cell samplesPeripheral blood cell populationsImmune systemFraction of TregsRegulatory T cellsBlood mononuclear cellsBlood cell populationsFlow cytometry analysisImmune aberrationsIPF patientsTregsMononuclear cellsSingle-cell RNA sequencingLung homogenatesMonocyte chemoattractantRole of Noradrenaline and Macrophage Dynamics in Pulmonary Fibrosis
Ishikawa G, Peng X, Mcgovern J, Ghincea A, Saber T, Sun H, Sauler M, Ryu C, Herzog E. Role of Noradrenaline and Macrophage Dynamics in Pulmonary Fibrosis. 2024, a5206-a5206. DOI: 10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a5206.Peer-Reviewed Original Research
2023
Toll-like Receptor-9 Activation Promotes Persistent Inflammation in the Lung During Influenza Infection
Essayas H, Kim J, Mcgovern J, Peng X, Cai Y, Ishikawa G, Herzog E, Dela Cruz C, Ryu C, Sharma L. Toll-like Receptor-9 Activation Promotes Persistent Inflammation in the Lung During Influenza Infection. 2023, a5608-a5608. DOI: 10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a5608.Peer-Reviewed Original Researchα1 Adrenoreceptor antagonism mitigates extracellular mitochondrial DNA accumulation in lung fibrosis models and in patients with idiopathic pulmonary fibrosis
Ishikawa G, Peng X, McGovern J, Woo S, Perry C, Liu A, Yu S, Ghincea A, Kishchanka A, Fiorini V, Hu B, Sun Y, Sun H, Ryu C, Herzog E. α1 Adrenoreceptor antagonism mitigates extracellular mitochondrial DNA accumulation in lung fibrosis models and in patients with idiopathic pulmonary fibrosis. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2023, 324: l639-l651. PMID: 36648147, PMCID: PMC10110730, DOI: 10.1152/ajplung.00119.2022.Peer-Reviewed Original ResearchConceptsAdrenergic nerve supplyIdiopathic pulmonary fibrosisΑ1 adrenoreceptorsPulmonary fibrosisNerve supplyCultured normal human lung fibroblastsInnate immune ligandsLung fibrosis modelNormal human lung fibroblastsSmooth muscle actinHuman lung fibroblastsAdrenal resectionAdrenoreceptor antagonismExtracellular mtDNAIPF cohortImproved survivalΑ1-adrenoreceptor antagonistsLung fibrosisAdrenal sourceFibroblast accumulationAdrenoreceptor antagonistBleomycin modelFibrosis modelLung fibrogenesisMouse model
2022
PTX3 in Granuloma Formation and Sarcoidosis: Helping Macrophages Accept a “Complement”
Ishikawa G, Herzog EL. PTX3 in Granuloma Formation and Sarcoidosis: Helping Macrophages Accept a “Complement”. American Journal Of Respiratory And Critical Care Medicine 2022, 206: 1064-1065. PMID: 35820078, PMCID: PMC9704837, DOI: 10.1164/rccm.202207-1277ed.Commentaries, Editorials and Letters
2021
Evolving Perspectives on Innate Immune Mechanisms of IPF
Ishikawa G, Liu A, Herzog EL. Evolving Perspectives on Innate Immune Mechanisms of IPF. Frontiers In Molecular Biosciences 2021, 8: 676569. PMID: 34434962, PMCID: PMC8381017, DOI: 10.3389/fmolb.2021.676569.Peer-Reviewed Original ResearchIdiopathic pulmonary fibrosisInnate immunityInnate immune populationsMolecular patternsMyeloid suppressor cellsInnate lymphoid cellsInnate immune mechanismsEpithelial-fibroblast interactionsRole of substancesSuppressor cellsPulmonary fibrosisImmune populationsImmune mechanismsDisease outcomePotential therapyLymphoid cellsHuman studiesFibrotic microenvironmentCommensal microbesAnimal modelingGenetic factorsImmunityFuture studiesComplex roleCellsElevated IL-15 concentrations in the sarcoidosis lung are independent of granuloma burden and disease phenotypes
Minasyan M, Sharma L, Pivarnik T, Liu W, Adams T, Bermejo S, Peng X, Liu A, Ishikawa G, Perry C, Kaminski N, Gulati M, Herzog EL, Dela Cruz CS, Ryu C. Elevated IL-15 concentrations in the sarcoidosis lung are independent of granuloma burden and disease phenotypes. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2021, 320: l1137-l1146. PMID: 33851886, PMCID: PMC8285626, DOI: 10.1152/ajplung.00575.2020.Peer-Reviewed Original ResearchConceptsIL-15 concentrationsIL-15Bronchoalveolar lavageDisease pathogenesisSarcoidosis lungClinical manifestationsLineages of miceIL-15 receptor αHuman cohortsInflammation of sarcoidosisIL-15 levelsOngoing inflammatory processSystemic granulomatous diseaseNumber of granulomasDisease phenotypeSarcoidosis cohortTDM administrationGranuloma numberComorbid conditionsClinical progressionInterleukin-15Granulomatous diseaseInflammatory processGranuloma formationHealthy controls
Academic Achievements & Community Involvement
Clinical Care
Overview
Genta Ishikawa, MD, is a pulmonologist who cares for people with interstitial lung disease, including pulmonary fibrosis, a form of lung scarring. He also provides critical care support for patients who experience severe respiratory challenges.
As an instructor at Yale School of Medicine, Dr. Ishikawa studies how nerve-derived chemicals such as noradrenaline influence lung scarring, with the goal of discovering new ways to slow or halt disease progression.
Dr. Ishikawa earned his medical degree from Hokkaido University in Japan and completed a master of public health at Emory University. He went on to finish a residency in internal medicine and a fellowship in pulmonary, critical care, and sleep medicine at Mount Sinai in New York, followed by a postdoctoral fellowship at Yale School of Medicine.
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Pulmonary, Critical Care & Sleep Medicine
300 Cedar Street, P.O. Box 208057
New Haven, CT 06520
United States