Search results for "Inflammatory cytokine"

showing 10 items of 464 documents

Mitochondrial Alterations and Enhanced Human Leukocyte/Endothelial Cell Interactions in Type 1 Diabetes

2020

Type 1 diabetes has been associated with oxidative stress. This study evaluates the rates of oxidative stress, mitochondrial function, leukocyte&ndash

Mitochondrial ROScardiovascular riskmedicine.medical_specialtyendotheliumtype 1 diabeteslcsh:Medicine030209 endocrinology & metabolism030204 cardiovascular system & hematologyMitochondrionmedicine.disease_causeArticleProinflammatory cytokineSuperoxide dismutase03 medical and health sciences0302 clinical medicineInternal medicinemedicinechemistry.chemical_classificationReactive oxygen speciesbiologyCell adhesion moleculebusiness.industrylcsh:RGeneral MedicinemitochondriaEndocrinologychemistryinflammationMyeloperoxidasebiology.proteinbusinessOxidative stressJournal of Clinical Medicine
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Neuronal injury in chronic CNS inflammation.

2010

Introduction Multiple sclerosis (MS) is the most common chronic inflammatory disease of the central nervous system which is characterized by inflammatory demyelination and neurodegeneration. Neurological symptoms include sensory disturbances, optic neuritis, limb weakness, ataxia, bladder dysfunction, cognitive deficits and fatigue. Pathophysiology The inflammation process with MS is promoted by several inflammatory cytokines produced by the immune cells themselves and local resident cells like activated microglia. Consecutive damaging pathways involve the transmigration of activated B lymphocytes and plasma cells, which synthesize antibodies against the myelin sheath, boost the immune atta…

Multiple SclerosisInflammationNeuroprotectionSeverity of Illness IndexProinflammatory cytokineCentral Nervous System DiseasesmedicineAnimalsHumansRemyelinationNeuroinflammationInflammationNeuronsMicrogliabusiness.industryMultiple sclerosismedicine.diseaseAstrogliosisAnesthesiology and Pain Medicinemedicine.anatomical_structureNeuroprotective AgentsImmunologyChronic DiseaseMicrogliamedicine.symptomInflammation MediatorsbusinessBest practiceresearch. Clinical anaesthesiology
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NFAT1 deficit and NFAT2 deficit attenuate EAE via different mechanisms

2015

EAE serves as an animal model for multiple sclerosis and is initiated by autoreactive T cells that infiltrate the CNS. Recognition of myelin-associated Ags within the CNS leads to activation of the transcription factor family NFAT. Here, we demonstrate an essential role for NFAT in disease induction, as the combined lack of NFAT1 (NFATc2) and NFAT2 (NFATc1) completely protected mice. Single deficiency of either NFAT1 or NFAT2 ameliorated the course of EAE, and NFAT2 ablation resulted in an obstructed proinflammatory reaction. However, NFAT1 deficit led to an anti-inflammatory response with nonpathogenic Th17 and Th2 cells concurrently secreting IL-17, IL-4, and IL-10. Both IL-4 and IL-10 co…

Multiple sclerosismedicine.medical_treatmentImmunologyLymphokineImmunosuppressionNFATBiologymedicine.diseasemedicine.disease_causeAutoimmunityBlockadeProinflammatory cytokineImmunologymedicineImmunology and AllergyTranscription factorEuropean Journal of Immunology
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Antibodies to proteinase 3 mediate expression of vascular cell adhesion molecule-1 (VCAM-1).

1996

SUMMARY VCAM-1 was first identified as an adhesion molecule induced on human endothelial cells (HEC) by inflammatory cytokines such as IL-1, tumour necrosis factor (TNF), and lipopolysaccharide (LPS). The molecule binds to a variety of leucocytes, including B cells, T cells, basophils, eosinophils and monocytes. Vascular expression of VCAM-1 has been associated with a number of disease states, including rheumatoid arthritis and vasculitis. The detection of antineutrophil cytoplasmic antibodies (ANCA), especially to proteinase 3 (PR3), has become important in the diagnosis of Wegener’s granulomatosis (WG) and related vasculitides. Recently we were able to demonstrate a direct effect of anti-…

MyeloblastinT-LymphocytesImmunologyMolecular Sequence DataVascular Cell Adhesion Molecule-1BiologyAntibodiesProinflammatory cytokinechemistry.chemical_compoundAntigenProteinase 3Cell AdhesionImmunology and AllergyHumanscardiovascular diseasesRNA MessengerVCAM-1Cell adhesionCells CulturedBase SequenceCell adhesion moleculeSerine EndopeptidasesOriginal ArticleschemistryImmunologybiology.proteinTumor necrosis factor alphaEndothelium VascularAntibodyClinical and experimental immunology
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Cutting Edge: IL-1α Is a Crucial Danger Signal Triggering Acute Myocardial Inflammation during Myocardial Infarction

2016

Abstract Myocardial infarction (MI) induces a sterile inflammatory response that contributes to adverse cardiac remodeling. The initiating mechanisms of this response remain incompletely defined. We found that necrotic cardiomyocytes released a heat-labile proinflammatory signal activating MAPKs and NF-κB in cardiac fibroblasts, with secondary production of cytokines. This response was abolished in Myd88−/− fibroblasts but was unaffected in nlrp3-deficient fibroblasts. Despite MyD88 dependency, the response was TLR independent, as explored in TLR reporter cells, pointing to a contribution of the IL-1 pathway. Indeed, necrotic cardiomyocytes released IL-1α, but not IL-1β, and the immune acti…

MyocarditisImmunologyInterleukin-1betaMyocardial InfarctionInflammation030204 cardiovascular system & hematologyArticleProinflammatory cytokine03 medical and health sciencesMice0302 clinical medicineImmune system[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemIn vivoInterleukin-1alphamedicineImmunology and AllergyAnimalsMyocytes CardiacMyocardial infarction030304 developmental biologyInflammationMice Knockout0303 health sciencesbusiness.industryToll-Like Receptorsmedicine.disease[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemMyocarditisIL1AImmunologyMyeloid Differentiation Factor 88Cancer researchmedicine.symptomSignal transductionbusinessSignal Transduction
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Hypoxia induces proinflammatory cytokines production in alpha-1 antitrypsin deficiency patients

2021

Introduction: Alpha-1 antitrypsin deficiency (AATD) is a rare respiratory condition characterized by abnormal inflammation, where neutrophils play a key role. Excessive neutrophil activation leads to an increase in the oxygen (O2) intake, causing local hypoxia and increased tissue-injury capacity. Tissue hypoxia is part of the inflammatory process so neutrophils can function effectively under these conditions. However, the mechanisms by which neutrophils mediate tissue damage under hypoxia remain unclear. The study aimed to determine whether hypoxia modifies the cytokine profile in AATD patients. Methods: Neutrophils from 22 AATD patients (6 MZ; 9 SZ; 7 ZZ) and 7 controls (MM) were exposed …

NecrosisLungAlpha 1-antitrypsin deficiencybusiness.industrymedicine.medical_treatmentInflammationHypoxia (medical)medicine.diseaseProinflammatory cytokineCytokinemedicine.anatomical_structureImmunologyMedicineTumor necrosis factor alphamedicine.symptombusinessMolecular pathology and functional genomics
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Complex regional pain syndrome-significant progress in understanding.

2015

Research into complex regional pain syndrome (CRPS) has made significant progress. First, there was the implementation of the official IASP "Budapest" diagnostic criteria. It would be desirable to also define exclusion and outcome criteria that should be reported in studies. The next step was to recognize the complex pathophysiology. After trauma, some inflammation is physiological; in acute CRPS, this inflammation persists for months. There is an abundance of inflammatory and a lack of anti-inflammatory mediators. This proinflammatory network (cytokines and probably also other mediators) sensitizes the peripheral and spinal nociceptive system, it facilitates the release of neuropeptides fr…

Nervous systemInflammationNeuronal Plasticitybusiness.industryInflammationmedicine.diseaseProinflammatory cytokineAnesthesiology and Pain MedicineComplex regional pain syndromeNociceptionmedicine.anatomical_structureNeurologyNeuroplasticitymedicineNociceptorDisease ProgressionAnimalsHumansNeurology (clinical)Endothelial dysfunctionmedicine.symptombusinessNeuroscienceComplex Regional Pain SyndromesPain
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Pharmacology of Ischemia-Reperfusion. Translational Research Considerations.

2016

Ischemia-reperfusion (IRI) is a complex physiopathological mechanism involving a large number of metabolic processes that can eventually lead to cell apoptosis and ultimately tissue necrosis. Treatment approaches intended to reduce or palliate the effects of IRI are varied, and are aimed basically at: inhibiting cell apoptosis and the complement system in the inflammatory process deriving from IRI, modulating calcium levels, maintaining mitochondrial membrane integrity, reducing the oxidative effects of IRI and levels of inflammatory cytokines, or minimizing the action of macrophages, neutrophils, and other cell types. This study involved an extensive, up-to-date review of the bibliography …

NeutrophilsIschemiaApoptosis030204 cardiovascular system & hematologyPharmacologyurologic and male genital diseasesAntioxidantsProinflammatory cytokineTranslational Research Biomedical03 medical and health sciences0302 clinical medicinemedicineHumanscardiovascular diseasesIschemic PreconditioningOpiate alkaloidurogenital systemMechanism (biology)business.industryTumor Necrosis Factor-alphaMacrophagesOpiate AlkaloidsfungiNF-kappa BComplement System Proteinsmedicine.diseaseApoptosis030220 oncology & carcinogenesisReperfusion InjuryAnesthetics InhalationIschemic preconditioningCytokinesSurgeryTumor necrosis factor alphaInflammation MediatorsbusinessReperfusion injuryJournal of investigative surgery : the official journal of the Academy of Surgical Research
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Transplanting the genetic susceptibility to Crohn’s disease

2003

Susceptibility to Crohn’s disease may be transferred via haematopoietic stem cells, highlighting the pivotal role of genetic factors in the pathogenesis of Crohn’s disease Crohn’s disease (CD) is one of the two most common forms of inflammatory bowel disease (IBD). The prevalence of CD has increased in Western countries over the past decades and mainly young patients are affected, with a peak incidence between 15 and 35 years.1 The aetiology of IBD is still unclear and should be considered as multifactorial according to recent studies.2 Genetic factors seem to play a pathogenic role as well as environmental, infectious, and immunological factors. All of these different aetiological aspects …

Nod2 Signaling Adaptor ProteinCase ReportBiologyInflammatory bowel diseaseProinflammatory cytokinePathogenesisImmune systemCrohn DiseasemedicineGenetic predispositionHumansGenetic Predisposition to DiseaseCrohn's diseasePolymorphism GeneticGastroenterologyIntracellular Signaling Peptides and ProteinsT helper cellT-Lymphocytes Helper-Inducermedicine.diseaseHodgkin Diseasedigestive system diseasesmedicine.anatomical_structureImmunologyCommentaryStem cell5' Untranslated RegionsCarrier ProteinsStem Cell Transplantation
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Frailty syndrome is associated with changes in peripheral inflammatory markers in prostate cancer patients undergoing androgen deprivation therapy.

2019

To evaluate the role of peripheral inflammation (leukocyte differential count, the proinflammatory cytokines IL-beta, TNF-α, IL-6, IL-8, and the inflammatory markers fibrinogen and C-reactive protein [CRP]) in frailty syndrome in patients with prostate cancer (CaP) undergoing antiandrogen therapy (ADT).A total of 46 men between 51 and 92 years of age with CaP and receiving ADT were classified as frail, prefrail or robust according to the Fried scale. A geriatric assessment was performed, based on the Minimental State Examination for cognitive function, the Barthel index for basic activities of daily living, the Yesavage scale for geriatric depression, and the Athens insomnia scale. In addit…

OncologyMalemedicine.medical_specialtyUrologyFrailty syndrome030232 urology & nephrologyInflammationFibrinogenSeverity of Illness IndexProinflammatory cytokineAndrogen deprivation therapy03 medical and health sciencesProstate cancer0302 clinical medicineInternal medicinemedicineHumansLymphocyte CountAthens insomnia scaleGeriatric AssessmentAgedAged 80 and overFrailtybusiness.industryProstatic NeoplasmsAndrogen AntagonistsMiddle Agedmedicine.diseaseCross-Sectional StudiesOncology030220 oncology & carcinogenesisBiomarker (medicine)medicine.symptomInflammation Mediatorsbusinessmedicine.drugUrologic oncology
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