2019
Lack of correlation of virulence gene profiles of Staphylococcus aureus bacteremia isolates with mortality
Park K, Greenwood-Quaintance K, Cunningham S, Rajagopalan G, Chia N, Jeraldo P, Mandrekar J, Patel R. Lack of correlation of virulence gene profiles of Staphylococcus aureus bacteremia isolates with mortality. Microbial Pathogenesis 2019, 133: 103543. PMID: 31102653, DOI: 10.1016/j.micpath.2019.103543.Peer-Reviewed Original ResearchMeSH KeywordsAgedAged, 80 and overAnimalsBacteremiaBacterial AdhesionBase SequenceCell ProliferationDrug Resistance, BacterialFemaleHLA-DR3 AntigenHumansImmune EvasionMaleMethicillin-Resistant Staphylococcus aureusMiceMice, TransgenicMiddle AgedMinnesotaPolymerase Chain ReactionStaphylococcal InfectionsStaphylococcus aureusSuperantigensVirulenceVirulence FactorsConceptsMethicillin-susceptible S. aureusS. aureus bacteremiaAureus bacteremiaMedical CenterHLA-DR3 transgenic miceStaphylococcus aureus bacteremiaMinnesota Medical CenterLarge medical centerImmune evasion genesVirulence genesVirulence gene profilesNumber of deathsClinical dataClinical valueTransgenic miceClinical practiceIndividual PCR assaysWhole-genome sequencing analysisMortalitySAg genesSurvivorsLack of correlationBacteremiaWGS analysisFunctional assays
2017
Randomized Clinical Trial of a Combination of an Inhaled Corticosteroid and Beta Agonist in Patients at Risk of Developing the Acute Respiratory Distress Syndrome*
Festic E, Carr G, Cartin-Ceba R, Hinds R, Banner-Goodspeed V, Bansal V, Asuni A, Talmor D, Rajagopalan G, Frank R, Gajic O, Matthay M, Levitt J. Randomized Clinical Trial of a Combination of an Inhaled Corticosteroid and Beta Agonist in Patients at Risk of Developing the Acute Respiratory Distress Syndrome*. Critical Care Medicine 2017, 45: 798-805. PMID: 28240689, PMCID: PMC5392150, DOI: 10.1097/ccm.0000000000002284.Peer-Reviewed Original ResearchMeSH KeywordsAcademic Medical CentersAdministration, InhalationAdrenal Cortex HormonesAdrenergic beta-AgonistsAgedAged, 80 and overBiomarkersBudesonide, Formoterol Fumarate Drug CombinationDouble-Blind MethodDrug Therapy, CombinationFemaleHumansHypoxiaMaleMiddle AgedOxygenPatient AcuityRespiration, ArtificialRespiratory Distress SyndromeRisk FactorsUnited StatesConceptsAcute respiratory distress syndromeRespiratory distress syndromeBudesonide/formoterolDistress syndromeBeta agonistsMore patientsMechanical ventilationClinical trialsEarly treatmentFirst study drugAlveolar fluid clearanceEffective pharmacologic treatmentRandomized clinical trialsPlacebo bidCategorical changePlacebo groupStudy drugAdult patientsLung inflammationLung injuryPharmacologic treatmentPrimary outcomeMedian timeEmergency departmentImproved oxygenation
2014
Superantigens in Staphylococcus aureus isolated from prosthetic joint infection
Kim C, Karau M, Greenwood-Quaintance K, Tilahun A, David C, Mandrekar J, Patel R, Rajagopalan G. Superantigens in Staphylococcus aureus isolated from prosthetic joint infection. Diagnostic Microbiology And Infectious Disease 2014, 81: 201-207. PMID: 25619753, PMCID: PMC4336809, DOI: 10.1016/j.diagmicrobio.2014.11.007.Peer-Reviewed Original ResearchSuperantigen profiling of Staphylococcus aureus infective endocarditis isolates
Chung J, Karau M, Greenwood-Quaintance K, Ballard A, Tilahun A, Khaleghi S, David C, Patel R, Rajagopalan G. Superantigen profiling of Staphylococcus aureus infective endocarditis isolates. Diagnostic Microbiology And Infectious Disease 2014, 79: 119-124. PMID: 24745820, PMCID: PMC4031024, DOI: 10.1016/j.diagmicrobio.2014.03.009.Peer-Reviewed Original ResearchConceptsSuperantigen genesSplenocyte proliferationS. aureusStaphylococcus aureus infective endocarditisMethicillin-susceptible S. aureusMethicillin-resistant S. aureusInfective endocarditis casesEnzyme-linked immunosorbent assayStaphylococcal enterotoxin AInfective endocarditisEndocarditis casesSuperantigen productionMouse splenocyte proliferationPCR-positive isolatesTSST-1EndocarditisImmunosorbent assayEnterotoxin AStaphylococcus aureusAureusProliferationIsolatesMortalityGenes
2013
Low Incidence of Spontaneous Type 1 Diabetes in Non-Obese Diabetic Mice Raised on Gluten-Free Diets Is Associated with Changes in the Intestinal Microbiome
Marietta E, Gomez A, Yeoman C, Tilahun A, Clark C, Luckey D, Murray J, White B, Kudva Y, Rajagopalan G. Low Incidence of Spontaneous Type 1 Diabetes in Non-Obese Diabetic Mice Raised on Gluten-Free Diets Is Associated with Changes in the Intestinal Microbiome. PLOS ONE 2013, 8: e78687. PMID: 24236037, PMCID: PMC3827256, DOI: 10.1371/journal.pone.0078687.Peer-Reviewed Original ResearchConceptsGluten-free dietNon-obese diabetic (NOD) miceAnti-diabetogenic effectsIncidence of hyperglycemiaNOD miceType 1 diabetesIntestinal microbiomeDietary glutenDiabetic miceSpontaneous type 1 diabetesAkkermansia speciesIncidence of diabetesIncidence of T1DIncidence of T1D.Blood glucose levelsIntestinal microbiome compositionLower incidenceGlucose levelsHigh incidenceAnimal studiesGut microfloraGut microbiomeHyperglycemiaIncidenceMice
2012
Is HOT a Cool Treatment for Type 1 Diabetes?
Rajagopalan G, Kudva Y, David C. Is HOT a Cool Treatment for Type 1 Diabetes? Diabetes 2012, 61: 1664-1666. PMID: 22723274, PMCID: PMC3379652, DOI: 10.2337/db12-0527.Peer-Reviewed Original Research
2011
HLA-DR3 restricted T cell epitope mimicry in induction of autoimmune response to lupus-associated antigen SmD
Deshmukh U, Sim D, Dai C, Kannapell C, Gaskin F, Rajagopalan G, David C, Fu S. HLA-DR3 restricted T cell epitope mimicry in induction of autoimmune response to lupus-associated antigen SmD. Journal Of Autoimmunity 2011, 37: 254-262. PMID: 21868195, PMCID: PMC3372418, DOI: 10.1016/j.jaut.2011.07.002.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibody FormationAutoantibodiesAutoantigensAutoimmunityEpitopes, T-LymphocyteFemaleHLA-DR3 AntigenHumansHybridomasImmunizationLupus Erythematosus, SystemicLymphocyte ActivationMiceMice, TransgenicMolecular MimicryPeptidesProtein BindingSnRNP Core ProteinsStreptococcus agalactiaeT-LymphocytesVibrio choleraeConceptsSystemic lupus erythematosusHLA-DR3 transgenic miceT cell epitopesHLA-DR3T cellsEpitope levelCell epitopesTransgenic miceMolecular mimicryPathogenesis of SLET cell epitope mimicryAutoreactive T cell clonesT hybridomasHLA-DR3 miceMicrobial peptidesAutoreactive T cellsProduction of autoantibodiesT cell responsesT cell clonesLupus erythematosusLupus autoantigensAutoimmune responseAutoimmune disordersImmunized miceEpitope mimicry
2007
Renal Hemodynamic, Inflammatory, and Apoptotic Responses to Lipopolysaccharide in HO-1−/− Mice
Tracz M, Juncos J, Grande J, Croatt A, Ackerman A, Rajagopalan G, Knutson K, Badley A, Griffin M, Alam J, Nath K. Renal Hemodynamic, Inflammatory, and Apoptotic Responses to Lipopolysaccharide in HO-1−/− Mice. American Journal Of Pathology 2007, 170: 1820-1830. PMID: 17525251, PMCID: PMC1899452, DOI: 10.2353/ajpath.2007.061093.Peer-Reviewed Original ResearchConceptsHeme oxygenase-1Immune cellsNF-kappaBRenal cytokine expressionRenal hemodynamic responseRenal blood flowGene heme oxygenase-1Glomerular filtration rateHO-1 deficiencyBone marrow progenitorsWidespread apoptosisHO-1 geneRenal hemodynamicsSepsis syndromeSerum cytokinesSerum levelsTh1 cytokinesClinical outcomesTh2 cytokinesCytokine expressionFiltration rateInflammatory responseHemodynamic responseBlunted activationBlood flow
2006
Acute systemic immune activation following vaginal exposure to staphylococcal enterotoxin B—Implications for menstrual shock
Rajagopalan G, Smart M, Murali N, Patel R, David C. Acute systemic immune activation following vaginal exposure to staphylococcal enterotoxin B—Implications for menstrual shock. Journal Of Reproductive Immunology 2006, 73: 51-59. PMID: 17070600, DOI: 10.1016/j.jri.2006.06.007.Peer-Reviewed Original ResearchConceptsMenstrual toxic shock syndromeSystemic immune activationHLA class II transgenic miceStaphylococcal enterotoxin BII transgenic miceImmune activationToxic shock syndromeSuperantigenic exotoxinsShock syndromeVaginal administrationTransgenic miceAcute systemic inflammatory diseaseSystemic inflammatory diseaseToxic shock syndrome toxinPeripheral lymphoid organsSEB-reactiveVaginal exposureProinflammatory cytokinesConjunctival routeLeukocytic infiltrationProfound elevationInflammatory diseasesLymphoid organsStaphylococcal superantigensT cellsIL-10-deficiency unmasks unique immune system defects and reveals differential regulation of organ-specific autoimmunity in non-obese diabetic mice
Rajagopalan G, Kudva Y, Sen M, Marietta E, Murali N, Nath K, Moore J, David C. IL-10-deficiency unmasks unique immune system defects and reveals differential regulation of organ-specific autoimmunity in non-obese diabetic mice. Cytokine 2006, 34: 85-95. PMID: 16740391, DOI: 10.1016/j.cyto.2006.04.006.Peer-Reviewed Original ResearchConceptsOrgan-specific autoimmunityComplete Freund's adjuvantNOD miceRectal prolapseToll-like receptor 9 agonistSystemic inflammatory cytokine responsesTh1-type autoimmune diseaseNon-obese diabetic (NOD) micePotent anti-inflammatory cytokineCyclophosphamide-induced diabetesDiabetic NOD miceIL-10 deficiencyAnti-inflammatory cytokinesReceptor 9 agonistInflammatory cytokine responseImmune system defectsType 1 diabetesPathogen-free conditionsSplenic macrophage numbersAdoptive transferIL-10Cytokine responsesDiabetic miceFreund's adjuvantAutoimmune diseases
2003
Accelerated Diabetes in Rat Insulin Promoter-Tumor Necrosis Factor-α Transgenic Nonobese Diabetic Mice Lacking Major Histocompatibility Class II Molecules
Rajagopalan G, Kudva YC, Flavell RA, David CS. Accelerated Diabetes in Rat Insulin Promoter-Tumor Necrosis Factor-α Transgenic Nonobese Diabetic Mice Lacking Major Histocompatibility Class II Molecules. Diabetes 2003, 52: 342-347. PMID: 12540606, DOI: 10.2337/diabetes.52.2.342.Peer-Reviewed Original ResearchConceptsClass II moleculesNecrosis factorT cellsHLA class II associationsHuman type 1 diabetesMajor histocompatibility class II moleculesFunctional class II moleculesClass II associationsType 1 diabetesRat insulin promoterTumor necrosis factorLocal proinflammatory environmentIslets of LangerhansAccelerated diabetesNOD miceHLA-DQ8Proinflammatory environmentC57BL/6 miceTNF-alphaDiabetesDisease pathogenesisSignificant protectionMajor histocompatibility complex locusNeonatal expressionMice
2002
Modulation of insulitis and type 1 diabetes by transgenic HLA-DR3 and DQ8 in NOD mice lacking endogenous MHC class II
Kudva Y, Rajagopalan G, Raju R, Abraham R, Smart M, Hanson J, David C. Modulation of insulitis and type 1 diabetes by transgenic HLA-DR3 and DQ8 in NOD mice lacking endogenous MHC class II. Human Immunology 2002, 63: 987-999. PMID: 12392851, DOI: 10.1016/s0198-8859(02)00435-4.Peer-Reviewed Original ResearchConceptsType 1 diabetesEndogenous class II moleculesClass II moleculesHLA-DR3NOD miceHuman leukocyte antigen (HLA) transgenic miceTransgenic miceEndogenous MHC class IICyclophosphamide-induced diabetesIntra-islet infiltrationMultiple low dosesDouble transgenic miceGroups of miceMHC class IINonobese diabetic (NOD) backgroundTransgenic expressionSpontaneous diabetesDiabetic backgroundUnmanipulated miceDQ8DiabetesLow dosesClass IILess infiltrationMice