Featured Publications
Severe respiratory viral infection induces procalcitonin in the absence of bacterial pneumonia
Gautam S, Cohen AJ, Stahl Y, Toro P, Young GM, Datta R, Yan X, Ristic NT, Bermejo SD, Sharma L, Restrepo M, Dela Cruz CS. Severe respiratory viral infection induces procalcitonin in the absence of bacterial pneumonia. Thorax 2020, 75: 974-981. PMID: 32826284, DOI: 10.1136/thoraxjnl-2020-214896.Peer-Reviewed Original ResearchConceptsPure viral infectionBacterial coinfectionViral infectionInfluenza infectionSevere respiratory viral infectionsAbility of procalcitoninRetrospective cohort studyViral respiratory infectionsRespiratory viral infectionsMarker of severityRespiratory viral illnessSevere viral infectionsSpecificity of procalcitoninCharacteristic curve analysisCellular modelHigher procalcitoninProcalcitonin expressionElevated procalcitoninCohort studyViral illnessRespiratory infectionsAntibiotic administrationBacterial pneumoniaSevere diseaseProcalcitoninQuantification of bronchoalveolar neutrophil extracellular traps and phagocytosis in murine pneumonia
Gautam S, Stahl Y, Young GM, Howell R, Cohen AJ, Tsang DA, Martin T, Sharma L, Dela Cruz CS. Quantification of bronchoalveolar neutrophil extracellular traps and phagocytosis in murine pneumonia. American Journal Of Physiology - Lung Cellular And Molecular Physiology 2020, 319: l661-l669. PMID: 32783617, PMCID: PMC7642899, DOI: 10.1152/ajplung.00316.2020.Peer-Reviewed Original ResearchConceptsNeutrophil extracellular trapsAcute respiratory distress syndromeChronic obstructive pulmonary diseaseNeutrophil responseExtracellular trapsDysregulation of neutrophilsObstructive pulmonary diseaseRespiratory distress syndromeNeutrophil effector functionsEx vivo assaysBronchoalveolar neutrophilsSevere asthmaDistress syndromeLung neutrophilsPulmonary diseaseMurine pneumoniaMurine modelEffector functionsNeutrophil researchMouse lungCystic fibrosisMethodologic issuesMurine researchLungArray of diseases
2023
IFN-γ Is Protective in Cytokine Release Syndrome-associated Extrapulmonary Acute Lung Injury.
Sun Y, Hu B, Stanley G, Harris ZM, Gautam S, Homer R, Koff JL, Rajagopalan G. IFN-γ Is Protective in Cytokine Release Syndrome-associated Extrapulmonary Acute Lung Injury. American Journal Of Respiratory Cell And Molecular Biology 2023, 68: 75-89. PMID: 36125351, PMCID: PMC9817908, DOI: 10.1165/rcmb.2022-0117oc.Peer-Reviewed Original ResearchConceptsCytokine release syndromeAcute lung injuryExtrapulmonary acute lung injuryIFN-γ KO miceIL-17ALung injuryKO miceStaphylococcal enterotoxin BRelease syndromeIL-17A KO miceSevere acute lung injuryAcute respiratory distress syndromeSystemic T cell activationEnterotoxin BAdaptive T lymphocytesDR3 transgenic miceNeutralization of IFNRespiratory distress syndromeHuman leukocyte antigenRole of IFNT cell cytokinesJanus kinase inhibitorS100A8/A9T cell activationALI parameters
2018
A Slick Solution to a Sticky Problem
Gautam S, Sharma L, Dela Cruz CS, Spiegel DA. A Slick Solution to a Sticky Problem. Biochemistry 2018, 57: 5923-5924. PMID: 30289246, DOI: 10.1021/acs.biochem.8b00916.Commentaries, Editorials and Letters
2011
Type 2 inositol 1,4,5‐trisphosphate receptor modulates bile salt export pump activity in rat hepatocytes
Kruglov EA, Gautam S, Guerra MT, Nathanson MH. Type 2 inositol 1,4,5‐trisphosphate receptor modulates bile salt export pump activity in rat hepatocytes. Hepatology 2011, 54: 1790-1799. PMID: 21748767, PMCID: PMC3205211, DOI: 10.1002/hep.24548.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsATP Binding Cassette Transporter, Subfamily B, Member 11ATP-Binding Cassette TransportersBile Acids and SaltsBile CanaliculiCalciumCalcium SignalingCell Culture TechniquesCells, CulturedCholestasisCollagenDisease Models, AnimalHepatocytesInositol 1,4,5-Trisphosphate ReceptorsLipopolysaccharidesMaleProtein Processing, Post-TranslationalRatsRats, Sprague-DawleyConceptsBile salt secretionBSEP activityTrisphosphate receptorBile salt export pumpType II inositolSalt secretionPosttranslational regulationCell systemType 2 inositolCanalicular membraneCholesterol depletionIntrahepatic cholestasisConfocal immunofluorescenceFunctional polarityIntracellular calciumIsolated cell systemRat hepatocytesAnimal modelsSandwich cultureCollagen sandwich culturesPharmacologic inhibitionShort-term regulationCell membraneExport pumpSecretion
2008
ATP8B1 Deficiency Disrupts the Bile Canalicular Membrane Bilayer Structure in Hepatocytes, But FXR Expression and Activity Are Maintained
Cai S, Gautam S, Nguyen T, Soroka CJ, Rahner C, Boyer JL. ATP8B1 Deficiency Disrupts the Bile Canalicular Membrane Bilayer Structure in Hepatocytes, But FXR Expression and Activity Are Maintained. Gastroenterology 2008, 136: 1060-1069.e4. PMID: 19027009, PMCID: PMC3439851, DOI: 10.1053/j.gastro.2008.10.025.Peer-Reviewed Original ResearchMeSH Keywords4-Chloro-7-nitrobenzofurazanAdenosine TriphosphatasesAnimalsATP Binding Cassette Transporter, Subfamily B, Member 11ATP-Binding Cassette TransportersBile CanaliculiCaco-2 CellsChenodeoxycholic AcidDNA-Binding ProteinsGastrointestinal AgentsGene ExpressionHepatocytesHumansMultidrug Resistance-Associated Protein 2PhosphatidylserinesPhospholipid Transfer ProteinsRatsReceptors, Cytoplasmic and NuclearRNA, Small InterferingTranscription FactorsTransfectionConceptsAminophospholipid flippaseMessenger RNAMembrane bilayer structureCanalicular membraneFarnesoid X receptorRat hepatocytesSmall heterodimer partnerMembrane transportersNBD-phosphatidylserineHeterodimer partnerDeficiency disruptsLuminal accumulationMembrane disruptionRNAConflicting hypothesesRat cellsFlippaseProtein levelsProtein expressionX receptorExpressionBSEP functionATP8B1CellsMembrane