2013
Cytokine Response Signatures in Disease Progression and Development of Severe Clinical Outcomes for Leptospirosis
Reis EA, Hagan JE, Ribeiro GS, Teixeira-Carvalho A, Martins-Filho OA, Montgomery RR, Shaw AC, Ko AI, Reis MG. Cytokine Response Signatures in Disease Progression and Development of Severe Clinical Outcomes for Leptospirosis. PLOS Neglected Tropical Diseases 2013, 7: e2457. PMID: 24069500, PMCID: PMC3777885, DOI: 10.1371/journal.pntd.0002457.Peer-Reviewed Original ResearchConceptsSevere pulmonary hemorrhage syndromeIL-10IL-6Mild diseaseClinical outcomesIL-8Disease progressionSevere diseaseSerum cytokine responseDays of symptomsHospital-based surveillanceAnti-inflammatory cytokinesIL-6 levelsCase-control study designPulmonary hemorrhage syndromeSevere clinical outcomesMultiplex bead array assayNon-fatal casesLife-threatening outcomesBead array assayImmunopathogenic roleCytokine profileCytokine stormIL-17ANonfatal outcomes
2012
Semaphorin 7a+ Regulatory T Cells Are Associated with Progressive Idiopathic Pulmonary Fibrosis and Are Implicated in Transforming Growth Factor-β1–induced Pulmonary Fibrosis
Reilkoff RA, Peng H, Murray LA, Peng X, Russell T, Montgomery R, Feghali-Bostwick C, Shaw A, Homer RJ, Gulati M, Mathur A, Elias JA, Herzog EL. Semaphorin 7a+ Regulatory T Cells Are Associated with Progressive Idiopathic Pulmonary Fibrosis and Are Implicated in Transforming Growth Factor-β1–induced Pulmonary Fibrosis. American Journal Of Respiratory And Critical Care Medicine 2012, 187: 180-188. PMID: 23220917, PMCID: PMC3570653, DOI: 10.1164/rccm.201206-1109oc.Peer-Reviewed Original ResearchConceptsIdiopathic pulmonary fibrosisRegulatory T cellsProgressive idiopathic pulmonary fibrosisSEMA 7ATGF-β1Pulmonary fibrosisLung fibrosisT cellsMurine lungIL-10Bone marrow-derived cellsAdoptive transfer approachT-cell mediatorsMarrow-derived cellsTransforming Growth Factor-β1Murine lung fibrosisGrowth factor-β1Lung CD4Adoptive transferIL-17AIL-4Disease progressionSemaphorin 7ACD4Mouse model
2010
Circulating monocytes from systemic sclerosis patients with interstitial lung disease show an enhanced profibrotic phenotype
Mathai SK, Gulati M, Peng X, Russell TR, Shaw AC, Rubinowitz AN, Murray LA, Siner JM, Antin-Ozerkis DE, Montgomery RR, Reilkoff RA, Bucala RJ, Herzog EL. Circulating monocytes from systemic sclerosis patients with interstitial lung disease show an enhanced profibrotic phenotype. Laboratory Investigation 2010, 90: 812-823. PMID: 20404807, PMCID: PMC3682419, DOI: 10.1038/labinvest.2010.73.Peer-Reviewed Original ResearchConceptsInterstitial lung diseaseSSc-ILD patientsSSc-ILDIL-10Normal controlsProfibrotic cellsSystemic sclerosisLung diseaseCollagen-producing cellsMCP-1Profibrotic phenotypeSSc-related interstitial lung diseaseFlow cytometryPeripheral blood profilesSSc-ILD cohortsIL-10 secretionSystemic sclerosis patientsExpression of CD163Blood of patientsHealthy aged controlsCultured CD14Profibrotic characteristicsProfibrotic mediatorsTNF levelsSclerosis patients
2009
IL-10 Signaling Blockade Controls Murine West Nile Virus Infection
Bai F, Town T, Qian F, Wang P, Kamanaka M, Connolly TM, Gate D, Montgomery RR, Flavell RA, Fikrig E. IL-10 Signaling Blockade Controls Murine West Nile Virus Infection. PLOS Pathogens 2009, 5: e1000610. PMID: 19816558, PMCID: PMC2749443, DOI: 10.1371/journal.ppat.1000610.Peer-Reviewed Original ResearchConceptsIL-10 signalingIL-10WNV infectionWest Nile virusIL-10-deficient miceWest Nile virus infectionImportant cellular sourceSignificant human morbidityRNA flavivirusWNV pathogenesisInterleukin-10Antiviral cytokinesEtiologic rolePharmacologic blockadeDeficient miceT cellsVirus infectionPharmacologic meansTherapeutic strategiesViral infectionCellular sourceInfectionHuman morbidityNile virusMice
2001
Murine Lyme Disease: No Evidence for Active Immune Down-Regulation in Resolving or Subclinical Infection
Montgomery R, Wang X, Malawista S. Murine Lyme Disease: No Evidence for Active Immune Down-Regulation in Resolving or Subclinical Infection. The Journal Of Infectious Diseases 2001, 183: 1631-1637. PMID: 11343212, DOI: 10.1086/320703.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBorrelia burgdorferi GroupDisease Models, AnimalFemaleFluorescent Antibody TechniqueInterleukin-1Interleukin-12Lyme DiseaseMacrophage ActivationMacrophagesMiceMyocarditisPeritoneumReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSpecific Pathogen-Free OrganismsTumor Necrosis Factor-alphaConceptsActive diseaseAnti-inflammatory cytokine IL-10Proinflammatory cytokines IL-1Levels of proinflammatoryAnti-inflammatory cytokinesCytokine IL-10Double-label immunofluorescent stainingCytokines IL-1Reverse transcription-polymerase chain reaction analysisSemiquantitative reverse transcription-polymerase chain reaction (RT-PCR) analysisTranscription-polymerase chain reaction analysisInfected heartsIL-10IL-12Inflammatory activityCytokine expressionTumor necrosisLocal macrophagesIL-1Peritoneal cavitySubclinical infectionChain reaction analysisLevels of mRNAMacrophage activationImmune system