2020
Itaconate is an effector of a Rab GTPase cell-autonomous host defense pathway against Salmonella
Chen M, Sun H, Boot M, Shao L, Chang SJ, Wang W, Lam TT, Lara-Tejero M, Rego EH, Galán JE. Itaconate is an effector of a Rab GTPase cell-autonomous host defense pathway against Salmonella. Science 2020, 369: 450-455. PMID: 32703879, PMCID: PMC8020367, DOI: 10.1126/science.aaz1333.Peer-Reviewed Original Research
2016
A Bacterial Pathogen Targets a Host Rab-Family GTPase Defense Pathway with a GAP
Spanò S, Gao X, Hannemann S, Lara-Tejero M, Galán JE. A Bacterial Pathogen Targets a Host Rab-Family GTPase Defense Pathway with a GAP. Cell Host & Microbe 2016, 19: 216-226. PMID: 26867180, PMCID: PMC4854434, DOI: 10.1016/j.chom.2016.01.004.Peer-Reviewed Original ResearchConceptsAntimicrobial defenseCell-autonomous defense mechanismS. typhi infectionHuman pathogen Salmonella typhiExchange factor BLOC-3Host defense pathwaysTyphi infectionType III secretion effectorsIntracellular pathogensPotential broad roleVacuolar pathogensSalmonella typhiPotent strategySalmonella effectorsBacterial pathogensMiceS. typhimuriumDefense pathwaysDefense mechanismsPathogen targetsPathogensEffectorsPathwayBroader roleBLOC-3
2006
A MyD88-Deficient Mouse Model Reveals a Role for Nramp1 in Campylobacter jejuni Infection
Watson RO, Novik V, Hofreuter D, Lara-Tejero M, Galán JE. A MyD88-Deficient Mouse Model Reveals a Role for Nramp1 in Campylobacter jejuni Infection. Infection And Immunity 2006, 75: 1994-2003. PMID: 17194808, PMCID: PMC1865720, DOI: 10.1128/iai.01216-06.Peer-Reviewed Original ResearchConceptsJejuni infectionAdaptor protein myeloid differentiation factor 88Myeloid differentiation factor 88Most Toll-like receptorsMyD88-deficient miceDifferentiation factor 88Campylobacter jejuni infectionAdult immunocompetent miceToll-like receptorsMajor worldwide causeFactor 88Immunocompetent miceMouse modelMouse susceptibilityEnteric illnessWorldwide causeJejuni colonizationInfectionMiceC. jejuniCampylobacter jejuniPotential roleVirulence genesBacterial pathogensIsogenic derivativesCritical Role for NALP3/CIAS1/Cryopyrin in Innate and Adaptive Immunity through Its Regulation of Caspase-1
Sutterwala FS, Ogura Y, Szczepanik M, Lara-Tejero M, Lichtenberger GS, Grant EP, Bertin J, Coyle AJ, Galán JE, Askenase PW, Flavell RA. Critical Role for NALP3/CIAS1/Cryopyrin in Innate and Adaptive Immunity through Its Regulation of Caspase-1. Immunity 2006, 24: 317-327. PMID: 16546100, DOI: 10.1016/j.immuni.2006.02.004.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsApoptosis Regulatory ProteinsAutoimmune DiseasesCARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Cytoskeletal ProteinsEnzyme ActivationImmunity, InnateInterleukin-1LipopolysaccharidesMacrophagesMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinRNA, MessengerSalmonella typhimuriumShock, SepticToll-Like ReceptorsConceptsIL-1betaImpaired contact hypersensitivity responseCaspase-1NALP3-deficient miceContact hypersensitivity responseFamilial cold autoinflammatory syndromeCytokines IL-1alphaCaspase-1 functionMuckle-Wells syndromeCaspase-1 activationLipopolysaccharide-stimulated macrophagesContact hypersensitivityHypersensitivity responseIL-18Articular syndromeAutoinflammatory disordersAutoinflammatory syndromesIL-1alphaAdaptive immunityAdaptor molecule ASCCaspase-1 activation pathwayNALP3SyndromeActivation pathwayMice