2019
IFN-mediated negative feedback supports bacteria class-specific macrophage inflammatory responses
Gottschalk R, Dorrington M, Dutta B, Krauss K, Martins A, Uderhardt S, Chan W, Tsang J, Torabi-Parizi P, Fraser I, Germain R. IFN-mediated negative feedback supports bacteria class-specific macrophage inflammatory responses. ELife 2019, 8: e46836. PMID: 31385572, PMCID: PMC6684266, DOI: 10.7554/elife.46836.Peer-Reviewed Original ResearchConceptsContext-dependent regulationGram-positive speciesGram-negative bacteriaClass-specific mannerInflammatory responseRegulatory eventsMolecular mechanismsMacrophage inflammatory responseMouse macrophagesLigand pairsInnate immunityInflammatory cytokine productionMacrophage responseBacteriaRegulationSpecific pathogensIL-10Cytokine productionLung infectionProduction dynamicsInhibitory eventsSpeciesMacrophagesNegative feedbackInflammation dynamicsResident Macrophages Cloak Tissue Microlesions to Prevent Neutrophil-Driven Inflammatory Damage
Uderhardt S, Martins A, Tsang J, Lämmermann T, Germain R. Resident Macrophages Cloak Tissue Microlesions to Prevent Neutrophil-Driven Inflammatory Damage. Cell 2019, 177: 541-555.e17. PMID: 30955887, PMCID: PMC6474841, DOI: 10.1016/j.cell.2019.02.028.Peer-Reviewed Original ResearchConceptsTissue-resident macrophagesTissue homeostasisDiverse tissuesCell deathOrgan architectureIndividual cellsNeutrophil swarmsResident macrophagesDense swarmsLocal cell injuryIntravital imagingLocal disruptionParenchymal cell deathDynamic intravital imagingInescapable consequenceCell damageCell injuryHomeostasisMacrophagesCascadeInflammatory damageDamageCellsAccumulationDisruption
2008
Cathepsin B Is Involved in the Trafficking of TNF-α-Containing Vesicles to the Plasma Membrane in Macrophages
Ha S, Martins A, Khazaie K, Han J, Chan B, Kim S. Cathepsin B Is Involved in the Trafficking of TNF-α-Containing Vesicles to the Plasma Membrane in Macrophages. The Journal Of Immunology 2008, 181: 690-697. PMID: 18566436, DOI: 10.4049/jimmunol.181.1.690.Peer-Reviewed Original ResearchConceptsPlasma membraneIntracellular cathepsin B activityCathepsin BCathepsin B activityMouse bone marrow-derived macrophagesGene identification methodsBone marrow-derived macrophagesMarrow-derived macrophagesB activityEctopic expressionLysosomal cysteine proteinasesInnate immune responsePosttranslational processingCysteine proteinasesTNF-alphaVesiclesKey mediatorMembranePotent proinflammatory cytokineLess TNF-alphaChronic inflammatory diseaseMacrophagesMutagenesisGFPMicrobes
2006
G‐CSF‐mediated inhibition of JNK is a key mechanism for Lactobacillus rhamnosus‐induced suppression of TNF production in macrophages
Kim S, Sheikh H, Ha S, Martins A, Reid G. G‐CSF‐mediated inhibition of JNK is a key mechanism for Lactobacillus rhamnosus‐induced suppression of TNF production in macrophages. Cellular Microbiology 2006, 8: 1958-1971. PMID: 16889627, DOI: 10.1111/j.1462-5822.2006.00763.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBone Marrow CellsCell LineCytokinesEnterococcus faecalisEscherichia coliGranulocyte Colony-Stimulating FactorHumansInterleukin-10JNK Mitogen-Activated Protein KinasesLacticaseibacillus rhamnosusMacrophage ActivationMacrophagesMacrophages, PeritonealMiceMice, Inbred C57BLP38 Mitogen-Activated Protein KinasesPhosphorylationProbioticsSignal TransductionSTAT3 Transcription FactorTumor Necrosis Factor-alphaConceptsGranulocyte-colony stimulating factorTNF productionL. rhamnosus GGGr-1Rhamnosus GGReceptor knockout miceAnti-inflammatory effectsMonocytic cell line THP-1Human monocytic cell line THP-1Cell line THP-1Lipopolysaccharide-activated macrophagesActivation of STAT3C-Jun N-terminal kinaseImmunomodulatory effectsTumor necrosisImmunomodulatory propertiesKnockout miceParacrine routeStimulating factorMacrophagesTHP-1Subsequent inhibitionMouse macrophagesCulture supernatantsNovo protein synthesis