Search results for "Inflammation."

showing 10 items of 2627 documents

ANTI-INFLAMMATORY ACTIVITY OF HSP60 IN HUMAN BRONCHIAL EPITHELIAL CELLS AND ITS INVOLVEMENT IN CHRONIC OBSTRUCTIVE PULMUNARY DISEASE

Bronchial InflammationSettore BIO/16 - Anatomia UmanaChaperonopathieCOPDHSP60
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Cigarette smoke alters IL-33 expression and release in airway epithelial cells

2014

AbstractAirway epithelium is a regulator of innate immune responses to a variety of insults including cigarette smoke. Cigarette smoke alters the expression and the activation of Toll Like Receptor 4 (TLR4), an innate immunity receptor. IL-33, an alarmin, increases innate immunity Th2 responses. The aims of this study were to explore whether mini-bronchoalveolar lavage (mini-BAL) or sera from smokers have altered concentrations of IL-33 and whether cigarette smoke extracts (CSE) alter both intracellular expression (mRNA and protein) and release of IL-33 in bronchial epithelial cells. The role of TLR4 in the expression of IL-33 was also explored.Mini-BALs, but not sera, from smokers show red…

Bronchial epithelial cellLipopolysaccharidesBlotting WesternBronchiInflammationRespiratory MucosaBiologyReal-Time Polymerase Chain ReactionBronchoalveolar LavageImmunoenzyme TechniquesBronchial epithelial cell; COPD; Cigarette smoke; IL-33; InflammationSmokeacute lung injury cigarette smokeinterleukin 33medicineCOPDHumansRNA MessengerReceptorMolecular BiologyCells CulturedCell ProliferationInflammationToll-like receptorInnate immune systemReverse Transcriptase Polymerase Chain ReactionInterleukinsCigarette smokeFlow CytometryInterleukin-33Immunity Innaterespiratory tract diseasesCell biologyToll-Like Receptor 4Interleukin 33ImmunologyIL-33TLR4Molecular MedicineRespiratory epitheliummedicine.symptomIntracellularBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Eosinophil Cationic Protein in Nasal Secretions and Blood Serum in Grass-Pollen Allergic Rhinitis

1996

Concentration of the Eosinophil Cationic Protein (ECP) measured in different body fluids has been demonstrated to be a good marker of eosinophilic inflammation. In allergic asthma, ECP levels in both broncho-alveolar-lavage (BAL) fluid and serum can be used to monitor disease activity. In allergic rhinitis, the value of ECP determinations in serum and nasal secretions was not directly compared, so far. In the present study, ECP levels in blood serum (Se) and nasal secretions (NS) of grass pollen allergic and healthy individuals under pollen exposure were analyzed. Forty-three grass-pollen allergic subjects and 19 healthy volunteers were included. Grass-pollen counts were measured using Bur…

BudesonideEosinophil cationic proteinbusiness.industryeducationfood and beverages03 medical and health sciencesfluids and secretions0302 clinical medicineBlood serumOtorhinolaryngologyEosinophilic inflammation030220 oncology & carcinogenesisGrass pollenHealthy individualsHealthy volunteersImmunologyotorhinolaryngologic diseasesMedicine030223 otorhinolaryngologybusinessSymptom scoremedicine.drugAmerican Journal of Rhinology
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Th17 immunity in children with allergic asthma and rhinitis: a pharmacological approach

2013

Th17 cells and IL-17A play a role in the development and progression of allergic diseases. We analyzed the IL-17A levels in sputum supernatants (Ss), nasal wash (NW) and plasma (P) from Healthy Controls (HC) and children with Asthma/Rhinitis. We tested the expression of IL-17A, RORγ(t) and FOXP3 in peripheral blood T-lymphocytes from intermittent and mild-moderate asthma. The effect of Budesonide and Formoterol was tested "in vitro" on IL-17A, RORγ(t) and FOXP3 expression in cultured T-lymphocytes from mild-moderate asthma/persistent rhinitis patients, and on nasal and bronchial epithelial cells stimulated with NW and Ss from mild-moderate asthma/persistent rhinitis. Further, the effect of …

BudesonideMalePulmonologyIL 13 and AsthmaGene ExpressionAnti-asthmatic AgentBiochemistryPediatricsimmune system diseasesFormoterol FumarateMolecular Cell BiologyAnti-Asthmatic AgentsBudesonideChildCells CulturedMultidisciplinaryImmune System ProteinsQInterleukin-17RFOXP3Forkhead Transcription FactorsNuclear Receptor Subfamily 1 Group F Member 3EthanolaminesMedicineFemaleInterleukin 17medicine.symptommedicine.drugResearch ArticleRhinitis Allergic PerennialAdolescentScienceImmunologyPediatric PulmonologyInflammationAdministration InhalationmedicineHumansAdrenergic beta-2 Receptor AgonistsBiologyAsthmaInflammationbusiness.industryInterleukin-8SputumImmunityProteinsImmunologic Subspecialtiesmedicine.diseaseNasal Lavage FluidAsthmarespiratory tract diseasesCase-Control StudiesImmunologySputumTh17 CellsClinical ImmunologyFormoterolbusinessPulmonary Immunology
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Fighting mycobacterial infections by antibiotics, phytochemicals and vaccines.

2011

Buruli ulcer is a neglected disease caused by Mycobacterium ulcerans and represents the world's third most common mycobacterial infection. It produces the polyketide toxins, mycolactones A, B, C and D, which induce apoptosis and necrosis. Clinical symptoms are subcutaneous nodules, papules, plaques and ulcerating oedemae, which can enlarge and destroy nerves and blood vessels and even invade bones by lymphatic or haematogenous spread (osteomyelitis). Patients usually do not suffer from pain or systematic inflammation. Surgery is the treatment of choice, although recurrence is common and wide surgical excisions including healthy tissues result in significant morbidity. Antibiotic therapy wit…

Buruli ulcerNecrosismedicine.drug_classImmunologyAntibioticsBacterial ToxinsInflammationApoptosisQuinolonesMicrobiologyNecrosisBacterial ProteinsmedicineVaccines DNAAnimalsHumansBuruli UlcerbiologyMycobacterium ulceransbusiness.industryOsteomyelitisVaccinationNeglected DiseasesChaperonin 60medicine.diseasebiology.organism_classificationRifamycinsAnti-Bacterial AgentsVaccinationInfectious DiseasesLymphatic systemAminoglycosidesMycobacterium ulceransImmunologyBacterial VaccinesMacrolidesmedicine.symptombusinessPhytotherapyMicrobes and infection
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Inflammatory Chemokines Expression Variations and Their Receptors in APP/PS1 Mice

2021

Background: In Alzheimer’s disease (AD), an increase in inflammation is distinctive. Amyloid precursor protein plus presenilin-1 (APP/PS1 mice) is a model for this illness. Chemokines secreted by central nervous system (CNS) cells could play multiple important roles in AD. Data looking for the chemokines involved in inflammatory mechanisms are lacking. To understand the changes that occur in the inflammation process in AD, it is necessary to improve strategies to act on specific inflammatory targets. Objective: Chemokines and their receptors involved in phagocytosis, demyelination, chemotaxis, and coagulation were the objective of our study. Methods: Female APPswe/PS1 double-transgenic mice…

CCR1CCR2ChemokineCCR3CCR4Mice TransgenicCCL7Amyloid beta-Protein PrecursorMiceChemokine receptorAlzheimer Diseasemental disordersAnimalsInflammationAmyloid beta-PeptidesbiologyGeneral NeuroscienceBrainChemotaxisGeneral MedicineDisease Models AnimalPsychiatry and Mental healthClinical PsychologyImmunologybiology.proteinFemaleReceptors ChemokineChemokinesGeriatrics and GerontologyJournal of Alzheimer's Disease
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Systemic Inflammation in Metabolic Syndrome: Increased Platelet and Leukocyte Activation, and Key Role of CX3CL1/CX3CR1 and CCL2/CCR2 Axes in Arteria…

2019

Background: Metabolic syndrome is associated with low-grade systemic inflammation, which is a key driver of premature atherosclerosis. We characterized immune cell behavior in metabolic syndrome, its consequences, and the potential involvement of the CX3CL1/CX3CR1 and CCL2/CCR2 chemokine axes. Methods: Whole blood from 18 patients with metabolic syndrome and 21 age-matched controls was analyzed by flow cytometry to determine the leukocyte immunophenotypes, activation, platelet-leukocyte aggregates, and CX3CR1 expression. ELISA determined the plasma marker levels. Platelet-leukocyte aggregates adhesion to tumor necrosis factor-&alpha

CCR2Chemokinelcsh:Medicinechemokines030204 cardiovascular system & hematologySystemic inflammationArticlemetabolic syndromeendothelial dysfunctionProinflammatory cytokine03 medical and health sciences0302 clinical medicineleukocyte activationmedicineplatelet activationPlatelet activationEndothelial dysfunction030304 developmental biologysystemic inflammation0303 health sciencesbiologybusiness.industryMonocytelcsh:RGeneral Medicinemedicine.diseasecytokinesmedicine.anatomical_structureImmunologybiology.proteinTumor necrosis factor alphamedicine.symptombusinessJournal of Clinical Medicine
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The Cytokine GM-CSF Drives the Inflammatory Signature of CCR2+ Monocytes and Licenses Autoimmunity.

2015

Granulocyte-macrophage colony-stimulating factor (GM-CSF) has emerged as a crucial cytokine produced by auto-reactive T helper (Th) cells that initiate tissue inflammation. Multiple cell types can sense GM-CSF, but the identity of the pathogenic GM-CSF-responsive cells is unclear. By using conditional gene targeting, we systematically deleted the GM-CSF receptor (Csf2rb) in specific subpopulations throughout the myeloid lineages. Experimental autoimmune encephalomyelitis (EAE) progressed normally when either classical dendritic cells (cDCs) or neutrophils lacked GM-CSF responsiveness. The development of tissue-invading monocyte-derived dendritic cells (moDCs) was also unperturbed upon Csf2r…

CCR2Myeloidmedicine.medical_treatmentInterleukin-1betaAutoimmunitymedicine.disease_causeMonocytesAutoimmunityCytokine Receptor Common beta Subunit0302 clinical medicineSTAT5 Transcription FactorImmunology and AllergyAntigens LyMyeloid CellsPhosphorylationMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionExperimental autoimmune encephalomyelitisGene targetingFlow CytometryInfectious DiseasesCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factor2723 Immunology and Allergymedicine.symptommedicine.drugSignal TransductionEncephalomyelitis Autoimmune ExperimentalReceptors CCR2Immunology610 Medicine & healthInflammationMice TransgenicBiology03 medical and health sciencesmedicineAnimalsHumans030304 developmental biologyInflammation2403 ImmunologyGranulocyte-Macrophage Colony-Stimulating Factor2725 Infectious DiseasesDendritic Cellsmedicine.disease10040 Clinic for NeurologyImmunologyTranscriptome030217 neurology & neurosurgery
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Imaging of T cell-mediated inflammation in a preclinical GvHD model using radiolabeled anti-human CD3 antibody

2019

CD3 Antibodymedicine.anatomical_structurebusiness.industryT cellCancer researchMedicineInflammationmedicine.symptombusiness57. Jahrestagung der Deutschen Gesellschaft für Nuklearmedizin
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Generation of human pulmonary microvascular endothelial cell lines.

2001

The limited lifespan of human microvascular endothelial cells in cell culture represents a major obstacle for the study of microvascular pathobiology. To date, no endothelial cell line is available that demonstrates all of the fundamental characteristics of microvascular endothelial cells. We have generated endothelial cell lines from human pulmonary microvascular endothelial cells (HPMEC) isolated from adult donors. HPMEC were cotransfected with a plasmid encoding the catalytic component of telomerase (hTERT) and a plasmid encoding the simian virus 40 (SV40) large T antigen. Cells transfected with either plasmid alone had an extended lifespan, but the cultures eventually entered crisis aft…

CD31AdultLipopolysaccharidesPathologymedicine.medical_specialtyPulmonary CirculationTime FactorsEndotheliumAngiogenesisCell SurvivalCell TransplantationAntigens Polyomavirus TransformingTransplantation HeterologousMice NudeNeovascularization PhysiologicBiologyTransfectionPathology and Forensic MedicineCell LineMiceCatalytic DomainmedicineAnimalsHumansMolecular BiologyTelomeraseCells CulturedMatrigelPlatelet Endothelial Cell Adhesion MoleculeCell adhesion moleculeMicrocirculationCell BiologyCell biologyEndothelial stem cellDNA-Binding Proteinsmedicine.anatomical_structurePhenotypeCell cultureEndothelium VascularInflammation MediatorsBiomarkersCell DivisionPlasmidsLaboratory investigation; a journal of technical methods and pathology
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