Search results for "Alveolar macrophage"

showing 8 items of 8 documents

Cigarette smoke promotes inflammasome‐independent activation of caspase‐1 and ‐4 leading to gasdermin D cleavage in human macrophages

2022

Mechanisms and consequences of gasdermin D (GSDMD) activation in cigarette smoke (CS)-associated inflammation and lung disease are unknown. GSDMD is a downstream effector of caspase-1, -8, and -4. Upon cleavage, GSDMD generates pores into cell membranes. Different degrees of GSDMD activation are associated with a range of physiological outputs ranging from cell hyperactivation to pyroptosis. We have previously reported that in human monocyte-derived macrophages CS extract (CSE) inhibits the NLRP3 inflammasome and shifts the response to lipopolysaccharide (LPS) towards the TLR4-TRIF axis leading to activation of caspase-8, which, in turn, activates caspase-1. In the present work, we investig…

InflammationLipopolysaccharidesPore Forming Cytotoxic Proteinsalveolar macrophages caspasecigarette smoke inflammasome lung Caspase 1 Caspases Caspases Initiator Humans Inflammation Intracellular Signaling Peptides and Proteins Lipopolysaccharides Lipopolysaccharides NLR Family Pyrin Domain-Containing 3 Protein Phosphate-Binding Proteins Pore Forming Cytotoxic Proteins Tobacco Cigarette Smoking Inflammasomes.InflammasomesSettore BIO/16 - Anatomia UmanaMacrophagesCaspase 1Intracellular Signaling Peptides and ProteinsPhosphate-Binding ProteinsBiochemistryCaspases InitiatorCigarette SmokingCaspasesNLR Family Pyrin Domain-Containing 3 ProteinTobaccoGeneticsHumansMolecular BiologyBiotechnologyThe FASEB Journal
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Endogenous nitric oxide inhibits leukotriene B4 release from rat alveolar macrophages

1997

Effects of endogenous nitric oxide (NO) on the release of mediators of the lipoxygenase and cyclo-oxygenase pathway from rat alveolar macrophages were studied. Alveolar macrophages, freshly isolated or after 18-h culture, were incubated in (amino acid-free) Krebs medium and labelled with [3H]arachidonic acid. The release of [3H]leukotriene B4 and [3H]prostanoids (separated by high performance liquid chromatography) was determined. A 23187 was used as stimulus, as rising intracellular Ca2+ activates directly the phospholipase A2 and lipoxygenase pathway. A 23187 (10 microM) enhanced [3H]leukotriene B4 release from freshly prepared alveolar macrophages about 65-fold, but only 5- to 6-fold fro…

Leukotriene B4LipoxygenaseArachidonic AcidsBiologyNitric OxideLeukotriene B4Nitric oxideRats Sprague-Dawleychemistry.chemical_compoundLipoxygenasePhospholipase A2Macrophages AlveolarmedicineAnimalsEnzyme InhibitorsCalcimycinCells CulturedChromatography High Pressure LiquidPharmacologyomega-N-MethylarginineProstanoidMolecular biologyRatsmedicine.anatomical_structurechemistryBiochemistryProstaglandin-Endoperoxide SynthasesAlveolar macrophagebiology.proteinFemaleArachidonic acidNitric Oxide SynthasePulmonary alveolusEuropean Journal of Pharmacology
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CD11c+ Alveolar Macrophages are a Source of IL-23 During Lipopolysaccharide-Induced Acute Lung Injury

2013

Acute lung injury (ALI) is a severe pulmonary disease causing high numbers of fatalities worldwide. Innate immune responses are an integral part of the pathophysiologic events during ALI. Interleukin 23 (IL-23) is a proinflammatory mediator known to direct the inflammatory responses in various settings of infection, autoimmunity, and cancer. Interleukin 23 has been associated with proliferation and effector functions in T(H)17 cells. Surprisingly, little is known about production of IL-23 during ALI. In this study, we found expression of mRNA for IL-23p19 to be 10-fold elevated in lung homogenates of C57BL/6 mice after lipopolysaccharide (LPS)-induced ALI. Likewise, concentrations of IL-23 …

LipopolysaccharidesMaleLipopolysaccharideAcute Lung InjuryCD11cBiologyLung injuryCritical Care and Intensive Care MedicineInterleukin-23ArticleProinflammatory cytokineMicechemistry.chemical_compoundMacrophages AlveolarmedicineAnimalsInnate immune systemmedicine.diagnostic_testrespiratory systemCD11c Antigenrespiratory tract diseasesBronchoalveolar lavagechemistryImmunologyEmergency MedicineAlveolar macrophageInterleukin 17Shock
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Alveolar macrophage dynamics in murine lung regeneration

2012

In most mammalian species, the removal of one lung results in dramatic compensatory growth of the remaining lung. To investigate the contribution of alveolar macrophages (AMs) to murine post-pneumonectomy lung growth, we studied bronchoalveolar lavage (BAL)-derived AM on 3, 7, 14 and 21 days after left pneumonectomy. BAL demonstrated a 3.0-fold increase in AM (CD45(+), CD11b(-), CD11c(+), F4/80(+), Gr-1(-)) by 14 days after pneumonectomy. Cell cycle flow cytometry of the BAL-derived cells demonstrated an increase in S + G2 phase cells on days 3 (11.3 ± 2.7%) and 7 (12.1 ± 1.8%) after pneumonectomy. Correspondingly, AM demonstrated increased expression of VEGFR1 and MHC class II between days…

MHC class IIeducation.field_of_studyLungbiologymedicine.diagnostic_testPhysiologymedicine.medical_treatmentClinical BiochemistryPopulationCD11cCell Biologyrespiratory systemFlow cytometryAndrologyPneumonectomyBronchoalveolar lavagemedicine.anatomical_structureImmunologyAlveolar macrophagebiology.proteinmedicineeducationJournal of Cellular Physiology
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In vitro study of human alveolar macrophage and peripheral blood mononuclear cell reactive oxygen-intermediates release induced by sulfur dioxide at …

1994

Sulfur dioxide (SO2) is a major air pollutant in urban areas. Alveolar macrophages (AM) located on the alveolar surface are in direct contact with this inhaled gas. We evaluated the dose-dependent effect of SO2 exposure on the oxidative metabolism of AM and peripheral blood mononuclear cells (PBMNC) by measuring the spontaneous and stimulated reactive oxygen intermediates (ROI) release. AM or PBMNC were placed on a polycarbonate membrane, which was in direct contact with the surface of a nutrient reservoir. For exposure of the cells to SO2 a special chamber was employed, in which humidified standard air with 5% CO2 at 37 degrees C was mixed with SO2 at the desired concentration. Periods of …

MalePulmonary and Respiratory MedicineTime Factorschemistry.chemical_elementStimulationIn Vitro Techniquescomplex mixturesOxygenPeripheral blood mononuclear cellchemistry.chemical_compoundMacrophages AlveolarHumansSulfur DioxideIn vitro studyCells CulturedSulfur dioxidePollutantChromatographyDose-Response Relationship DrugChemistryMiddle Agedrespiratory tract diseasesLuminescent MeasurementsImmunologyLeukocytes MononuclearAlveolar macrophageFemaleReactive Oxygen SpeciesBronchoalveolar Lavage FluidPolycarbonate membraneLung
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Lung-restricted activation of the alveolar macrophage/monocyte system in pulmonary sarcoidosis.

1992

An activation of T-cells that is restricted to the lung has been demonstrated in pulmonary sarcoidosis. The role of blood monocytes (MO) and alveolar macrophages (AM) in this concept of compartmentalized inflammation has not yet been evaluated. In order to elucidate this question, we measured the release of tumor necrosis factor alpha (TNF alpha) and interleukin-1 (IL-1) by peripheral blood mononuclear cells (PBMNC) and AM in 43 patients with sarcoidosis (32 with active, 11 with inactive disease) without therapy and correlated the spontaneous monokine release to parameters of the T-cell alveolitis and the course of the disease. TNF alpha as well as IL-1 were spontaneously released by AM of …

Pulmonary and Respiratory MedicineInterleukin 2Lung Diseasesmedicine.medical_specialtyTime FactorsSarcoidosisLung Diseases/metabolism610 MedizinInflammationSarcoidosis/metabolismLymphocyte ActivationMacrophages Alveolar/secretionPeripheral blood mononuclear cellMonocytesInterleukin-1/secretionInternal medicineMacrophages AlveolarmedicineMacrophageHumansddc:610Receptors Interleukin-2/metabolismTumor Necrosis Factor-alpha/secretionbusiness.industryTumor Necrosis Factor-alphaMonocyteLeukocytes Mononuclear/secretionMonocytes/immunologyReceptors Interleukin-2Macrophage ActivationMonokinemedicine.anatomical_structureEndocrinologyImmunologyAlveolar macrophageLeukocytes MononuclearInterleukin-2Tumor necrosis factor alphamedicine.symptomInterleukin-2/secretionbusinessmedicine.drugInterleukin-1The American review of respiratory disease
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Metabolism via arginase or nitric oxide synthase: two competing arginine pathways in macrophages

2014

Macrophages play a major role in the immune system, both as antimicrobial effector cells and as immunoregulatory cells, which induce, suppress or modulate adaptive immune responses. These key aspects of macrophage biology are fundamentally driven by the phenotype of macrophage arginine metabolism that is prevalent in an evolving or ongoing immune response. M1 macrophages express the enzyme nitric oxide synthase (NOS), which metabolizes arginine to nitric oxide (NO) and citrulline. NO can be metabolized to further downstream reactive nitrogen species, while citrulline might be reused for efficient NO synthesis via the citrulline-NO cycle. M2 macrophages are characterized by expression of the…

lcsh:Immunologic diseases. AllergyArginineMOUSE MACROPHAGESImmunologyReview ArticlemacrophageM1 and M2BiologyArginineamino acid transporterchemistry.chemical_compoundImmune systemALTERNATIVELY ACTIVATED MACROPHAGESCitrullineImmunology and AllergyMacrophageALVEOLAR MACROPHAGESIN-VIVOReactive nitrogen speciesMARROW-DERIVED MACROPHAGESScience & TechnologyT-CELL RESPONSESMOLECULAR-CLONINGArginaseImmunoregulationAcquired immune systemM2 MacrophageArginaseTUMOR-ASSOCIATED MACROPHAGESchemistryBiochemistryMURINE MACROPHAGESAMINO-ACID TRANSPORTERSNitric Oxide Synthaselcsh:RC581-607Life Sciences & BiomedicineFrontiers in Immunology
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Oxidative stress-induced glucocorticoid resistance is prevented by dual PDE3/PDE4 inhibition in human alveolar macrophages

2011

Summary Background Oxidative stress is present in airway diseases such as severe asthma or Chronic Obstructive Pulmonary Disease and contributes to the low response to glucocorticoids through the down-regulation of histone deacetylase (HDAC) activity. Objective To study the effects of the phosphodiesterase (PDE)-3 and 4 inhibitors and their combination vs. glucocorticoids in a model of lipopolysaccharide (LPS)-induced cytokine release in alveolar macrophages under oxidative stress conditions. Methods Differentiated U937 or human alveolar macrophages were stimulated with H2O2 (10–1000 μm) or cigarette smoke extract (CSE, 0–15%) for 4 h before LPS (0.5 μg/mL, 24 h) addition. In other experime…

medicine.medical_specialtymedicine.medical_treatmentImmunologyPhosphodiesterase 3Biologymedicine.disease_causeEndocrinologyCytokineInternal medicinemedicineAlveolar macrophageImmunology and AllergyCytokine secretionDexamethasoneGlucocorticoidOxidative stressRoliprammedicine.drugClinical & Experimental Allergy
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