Search results for "Macrophages"

showing 10 items of 533 documents

Release of transforming growth factor-beta (TGF-β) and fibronectin by alveolar macrophages in airway diseases

1996

Abstract Asthma and chronic bronchitis are associated with airway remodelling, and airway macrophages are present in bronchial inflammation. TGF-β and fibronectin released by alveolar macrophages possess a fibrogenic potency. The potential role of alveolar macrophages in airway remodelling was studied in asthma and chronic bronchitis by the release of TGF-β and fibronectin. Alveolar macrophages were isolated by bronchoalveolar lavage in 14 control subjects, 14 asthmatics and 14 chronic bronchitics. The spontaneous and lipopolysaccharide (LPS)- or concanavalin A (Con A)-induced release of TGF-β and fibronectin was measured by ELISA. Alveolar macrophages from chronic bronchitics spontaneously…

AdultLipopolysaccharidesMaleChronic bronchitisLipopolysaccharideImmunologyPathogenesischemistry.chemical_compoundFibrosisTransforming Growth Factor betaMacrophages AlveolarConcanavalin AImmunology and AllergyMacrophageMedicineHumansBronchitisbiologymedicine.diagnostic_testbusiness.industryOriginal Articlesrespiratory systemMiddle Agedmedicine.diseaseAsthmarespiratory tract diseasesFibronectinsFibronectinmedicine.anatomical_structureBronchoalveolar lavagechemistryImmunologyChronic Diseasebiology.proteinFemalePulmonary alveolusbusiness
researchProduct

Enzymatic modification of low-density lipoprotein in the arterial wall: a new role for plasmin and matrix metalloproteinases in atherogenesis.

2004

Objective— Functionally interactive proteases of the plasminogen/plasmin and the matrix metalloproteinase (MMP) system degrade and reorganize the extracellular matrix of the vessel wall in atherosclerosis. Here we investigated whether such proteases are able to confer atherogenic properties onto low density lipoprotein by nonoxidative modification. Methods and Results— Similar to the recently described enzymatically-modified low-density lipoprotein (E-LDL), native LDL exposed to plasmin or matrix MMP-2 or MMP-9 and cholesterylester-hydrolase (CEH) showed extensive deesterification, with ratios of free cholesterol to total cholesterol rising to 0.8 compared with 0.2 in native LDL. When the …

AdultLipoprotein modificationProteasesAdolescentPlasminArteriosclerosisBlotting WesternMatrix metalloproteinaseComplement Hemolytic Activity AssayMonocyteschemistry.chemical_compoundmedicineHumansTrypsinFibrinolysinComplement ActivationCells CulturedAgedbiologyMacrophagesAntibodies MonoclonalSodium Dodecyl SulfateLipoprotein(a)Middle AgedSterol EsteraseCell biologyLipoproteins LDLC-Reactive ProteinchemistryBiochemistryMatrix Metalloproteinase 9Low-density lipoproteinbiology.proteinMatrix Metalloproteinase 2lipids (amino acids peptides and proteins)Electrophoresis Polyacrylamide GelCardiology and Cardiovascular MedicinePlasminogen activatormedicine.drugLipoproteinArteriosclerosis, thrombosis, and vascular biology
researchProduct

Lung Compartmentalization of Increased TNF Releasing Ability by Mononuclear Phagocytes in Pulmonary Sarcoidosis

1989

The TNF is a monokine with cytotoxic and tumor-necrosing activities; in addition, TNF may play a role in inflammatory processes. The present study evaluates spontaneous and LPS-mediated release of TNF by AMs and autologous peripheral BMs of normal subjects and patients with pulmonary sarcoidosis. A recently developed cytotoxicity assay, specific for detection of TNF activity, was applied. This study demonstrates that (1) unstimulated mononuclear phagocytes released low levels of TNF with no differences between groups; (2) when effector cells were stimulated with LPS, AMs from patients with active pulmonary sarcoidosis released more TNF than AMs recovered from normal subjects and from patien…

AdultLung DiseasesMalePulmonary and Respiratory MedicineSarcoidosisCritical Care and Intensive Care MedicinePathogenesisHumansMedicineMacrophageLungLungTumor Necrosis Factor-alphabusiness.industryMacrophagesRespiratory diseaseMononuclear phagocyte systemCytotoxicity Tests Immunologicmedicine.diseasePulmonary AlveoliMonokinemedicine.anatomical_structureImmunologyLeukocytes MononuclearFemaleTumor necrosis factor alphaSarcoidosisCardiology and Cardiovascular MedicinebusinessBronchoalveolar Lavage FluidChest
researchProduct

Spontaneous Monokine Release by Alveolar Macrophages in Chronic Sarcoidosis

1991

In pulmonary sarcoidosis an activation of alveolar T lymphocytes and alveolar macrophages (AM) has been demonstrated. There is evidence that in contrast to acute disease a heightened T-cell response cannot be observed in the chronic phase of sarcoidosis. The role of AM in the inflammatory process of chronic sarcoidosis is not yet intensively evaluated. To address this question we measured the release of tumor necrosis factor alpha (TNFα) and interleukin-1 (IL-1) by AM of 39 patients with chronic sarcoidosis (duration > 4 years; 30 active, 9 inactive diseases) without therapy and correlated the monokine release with parameters of T-cell alveolitis and the course of the disease. The T4/T8 …

AdultLung DiseasesMaleSarcoidosisT-Lymphocytesmedicine.medical_treatmentImmunologyCD4-CD8 Ratio610 MedizinBronchoalveolar Lavage Fluid/immunologyTumor Necrosis Factor-alpha/biosynthesisLymphocyte Activation/immunologyLymphocyte ActivationMacrophages AlveolarmedicineHumansImmunology and AllergyMacrophageAntibodies Monoclonal/immunologyInterleukin-1/biosynthesisddc:610Tumor Necrosis Factor-alphabusiness.industryRespiratory diseaseAntibodies MonoclonalInterleukinGeneral MedicineT-Lymphocytes/immunologymedicine.diseaseSarcoidosis/immunologyMonokineLung Diseases/immunologyCytokinemedicine.anatomical_structureChronic DiseaseImmunologyMacrophages Alveolar/immunologyFemaleTumor necrosis factor alphaSarcoidosisPulmonary alveolusbusinessBronchoalveolar Lavage FluidInterleukin-1International Archives of Allergy and Immunology
researchProduct

Reduced Sympathetic Innervation in Endometriosis is Associated to Semaphorin 3C and 3F Expression

2016

Endometriosis is a chronic inflammatory disease and one of the most common causes of pelvic pain. The mechanisms underlying pain emergence or chronic inflammation during endometriosis remain unknown. Several chronic inflammatory diseases including endometriosis show reduced amounts of noradrenergic nerve fibers. The source of the affected innervation is still unclear. Semaphorins represent potential elicitors, due to their known role as axonal guidance cues, and are suggested as nerve repellent factors in different chronic inflammatory diseases. Therefore, semaphorins might influence the progress of neuroinflammatory mechanisms during endometriosis. Here, we analyzed the noradrenergic inner…

AdultMale0301 basic medicineNeuroimmunomodulationNeurogenesisEndometriosisNeuroscience (miscellaneous)EndometriosisPainInflammationSemaphorinsYoung Adult03 medical and health sciencesCellular and Molecular NeuroscienceNerve Fibers0302 clinical medicineImmune systemSemaphorinHumansMedicineSecretionEndometriosiReceptorbusiness.industryMacrophagesPelvic painInnervationNeurogenesisMiddle Agedmedicine.disease030104 developmental biologyNeurologyImmunologyFemaleSympathetic nerve fibermedicine.symptomSemaphorinCarrier Proteinsbusiness030217 neurology & neurosurgery
researchProduct

Both IL-12p70 and IL-23 are synthesized during active Crohnʼs disease and are down-regulated by treatment with anti-IL-12 p40 monoclonal antibody

2005

Background: Interleukin (IL)-12p70 and IL-23 are key T helper-1 (TH1) cytokines that drive the inflammation seen in numerous models of intestinal inflammation. These molecules contain an identical p40 chain that is bound to a p35 chain in IL-12 and a p19 chain in IL-23, making both potentially susceptible to modulation by an anti-IL-12p40 monoclonal antibody (mAb). Methods: In the present study, we sought to determine whether active inflammation in Crohn's disease (CD) is associated with the increased synthesis of both of these cytokines and whether patients treated with an anti-IL-12p40 mAb down-regulate IL-23 as well as IL-12p70 as previous reported. Results: To this end we initially dete…

AdultMaleAdolescentBiopsyT-Lymphocytesmedicine.medical_treatmentT cellDown-RegulationInterleukin-23Crohn DiseaseInterleukin 23medicineHumansImmunology and AllergyCells CulturedAgedLamina propriaMucous MembraneCD40biologyInterleukin-12 Subunit p40Interleukin-6InterleukinsMacrophagesGastroenterologyAntibodies MonoclonalInterleukinMiddle AgedInterleukin-12Protein Subunitsmedicine.anatomical_structureCytokineImmunologyInterleukin-23 Subunit p19biology.proteinInterleukin 12FemaleTumor necrosis factor alphaInterleukin-1Inflammatory Bowel Diseases
researchProduct

Evaluation of the prognostic role of tumour-associated macrophages in newly diagnosed classical hodgkin lymphoma and correlation with early FDG-PET a…

2017

In Hodgkin Lymphoma (HL), about 20% of patients still have relapsed/refractory disease and late toxic effects rate continue to rise with time. 'Early FDG-PET' and tissue macrophage infiltration (TAM) emerged as powerful prognostic predictors. The primary endpoint was to investigate the prognostic role of both early FDG-PET and TAM; the secondary endpoint was to test if early FDG-PET positivity could correlate with high TAM score. A cohort of 200 HL patients was analysed. Induction treatment plan consisted of two to six courses of ABVD and, if indicated, involved field radiation therapy. All patients repeated CT scan and FDG-PET after two cycles and after the completion of therapy. TAM in di…

AdultMaleAdolescentHodgkin’s lymphomaMacrophagePrognosiAntigens Differentiation MyelomonocyticVinblastineDisease-Free SurvivalCohort StudiesBleomycinYoung AdultAntigens CDFluorodeoxyglucose F18RecurrencePositron Emission Tomography Computed TomographyAntineoplastic Combined Chemotherapy ProtocolsHumansCD68AgedAged 80 and overHodgkin's lymphomahematologyMacrophagesCD68; Hodgkin's lymphoma; macrophages; PET; prognosis; hematology; oncology; cancer researchAntibodies MonoclonalMiddle AgedPrognosisHodgkin DiseaseImmunohistochemistryDacarbazineTreatment OutcomePETDoxorubicinPositron-Emission Tomographyoncologycancer researchFemaleNeoplasm Recurrence LocalFollow-Up Studies
researchProduct

Hypoxic macrophages impair autophagy in epithelial cells through Wnt1: relevance in IBD.

2014

A defective induction of epithelial autophagy may have a role in the pathogenesis of inflammatory bowel diseases. This process is regulated mainly by extracellular factors such as nutrients and growth factors and is highly induced by diverse situations of stress. We hypothesized that epithelial autophagy is regulated by the immune response that in turn is modulated by local hypoxia and inflammatory signals present in the inflamed mucosa. Our results reveal that HIF-1 alpha and Wnt1 were co-localized with CD68 in cells of the mucosa of IBD patients. We have observed increased protein levels of beta-catenin, phosphorylated mTOR, and p62 and decreased expression of LC3II in colonic epithelial …

AdultMaleAdolescentImmunologyWnt1 ProteinBiologyYoung AdultImmune systemAutophagyExtracellularHumansImmunology and AllergyIntestinal MucosaWNT1Wnt Signaling PathwayPI3K/AKT/mTOR pathwayRegulation of gene expressionCD68MacrophagesTOR Serine-Threonine KinasesAutophagyWnt signaling pathwayEpithelial CellsMiddle AgedHypoxia-Inducible Factor 1 alpha SubunitInflammatory Bowel DiseasesCell HypoxiaCell biologyGene Expression RegulationFemale
researchProduct

The monocytic population in chronic lymphocytic leukemia shows altered composition and deregulation of genes involved in phagocytosis and inflammatio…

2013

Macrophages reside in tissues infiltrated by chronic lymphocytic leukemia B cells and the extent of infiltration is associated with adverse prognostic factors. We studied blood monocyte population by flow cytometry and whole-genome microarrays. A mixed lymphocyte reaction was performed to evaluate proliferation of T cells in contact with monocytes from patients and normal donors. Migration and gene modulation in normal monocytes cultured with CLL cells were also evaluated. The absolute number of monocytes increased in chronic lymphocytic leukemia patients compared to the number in normal controls (792 +/- 86 cells/mu L versus 485 +/- 46 cells/mL, P=0.003). Higher numbers of non-classical CD…

AdultMaleCD14Chronic lymphocytic leukemiaPhagocytosisPopulationDown-RegulationInflammationMICROENVIRONMENTCD16BiologyTUMOR-ASSOCIATED MACROPHAGES; TIE2-EXPRESSING MONOCYTES; MICROENVIRONMENT; CLLMonocytesImmune systemPhagocytosismedicineHumanseducationCells CulturedAgedAged 80 and overInflammationeducation.field_of_studyMonocyteGene Expression ProfilingHematologyMiddle Agedmedicine.diseaseLeukemia Lymphocytic Chronic B-CellTIE2-EXPRESSING MONOCYTESGene Expression Regulation NeoplasticChronic Lymphocytic Leukemia; Monocyte; microenvironmentTUMOR-ASSOCIATED MACROPHAGESmedicine.anatomical_structureImmunologyFemalemedicine.symptomLymphocyte Culture Test MixedOriginal Articles and Brief ReportsCLLHaematologica
researchProduct

In Lysinuric Protein Intolerance system y+L activity is defective in monocytes and in GM-CSF-differentiated macrophages

2010

Abstract Background In the recessive aminoaciduria Lysinuric Protein Intolerance (LPI), mutations of SLC7A7/y+LAT1 impair system y+L transport activity for cationic amino acids. A severe complication of LPI is a form of Pulmonary Alveolar Proteinosis (PAP), in which alveolar spaces are filled with lipoproteinaceous material because of the impaired surfactant clearance by resident macrophages. The pathogenesis of LPI-associated PAP remains still obscure. The present study investigates for the first time the expression and function of y+LAT1 in monocytes and macrophages isolated from a patient affected by LPI-associated PAP. A comparison with mesenchymal cells from the same subject has been a…

AdultMaleCellular differentiationlcsh:MedicinePulmonary Alveolar ProteinosisBiologyMonocytesPathogenesisYoung AdultMacrophages AlveolarmedicineHumansGenetics(clinical)Pharmacology (medical)Amino Acid Metabolism Inborn ErrorsCells CulturedGenetics (clinical)Medicine(all)chemistry.chemical_classificationResearchFusion Regulatory Protein 1 Light ChainsLysinelcsh:RMesenchymal stem cellAmino Acid Transport System y+LGranulocyte-Macrophage Colony-Stimulating FactorCell DifferentiationGeneral Medicinemedicine.diseaseLysinuric protein intoleranceMolecular biologyAmino acidGranulocyte macrophage colony-stimulating factorchemistryAminoaciduriaImmunologyPulmonary alveolar proteinosismedicine.drugOrphanet Journal of Rare Diseases
researchProduct