Search results for "CYTOKINE"

showing 10 items of 1787 documents

Periodontitis and alzheimer´s disease

2020

Background Alzheimer's disease (AD), the main cause of dementia in the adult population, is characterized by a progressive loss of cognitive function. It is considered that neuroinflammation plays a fundamental role in its onset and progression. The bacteria present in the disbiotic microbiome generated during the course of periodontitis (PE) are capable of inducing a systemic inflammatory response, exacerbating the production of proinflammatory mediators that have the potential to spread to the systemic circulation. Material and Methods A literature review was made using the databases Scielo, PubMed, EBSCO and key words "Alzheimer disease", "Periodontitis", "Neurodegeneration", "Inflammati…

primary intraosseous squamous cell carcinomaInflammationDiseaseReviewProinflammatory cytokine03 medical and health sciences0302 clinical medicineAlzheimer DiseasemedicineDementiaHumansPeriodontologyPeriodontitisGeneral DentistryNeuroinflammationUNESCO:CIENCIAS MÉDICASAgedPeriodontitisInflammationbusiness.industryNeurodegenerationBrain030206 dentistrymedicine.diseaseodontogenic keratocystOtorhinolaryngologyImmunologyDisease ProgressionSurgeryprognosisAlzheimer's diseasemedicine.symptombusiness
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An Overview of Asthma and COVID-19: Protective Factors Against SARS-COV-2 in Pediatric Patients.

2021

Coronavirus disease 2019 (COVID-19) is a pandemic infectious disease caused by severe acute respiratory syndrome coronavirus SARS-COV-2. Aberrant innate immunity response and cytokine storm are responsible for the syndrome. Apparently, in asthmatic patients, the inadequate antiviral immune response and the tendency for asthma exacerbation evoked by common respiratory viruses could explain increased susceptibility to SARS-COV-2 infection. However, asthma has not been suggested to be a risk factor in COVID-19 patients. Therefore, in asthmatic patients some potential protective mechanisms against SARS-COV-2 have been hypothesized, like type 2 immune response, number of eosinophils, overproduct…

protective factorMini ReviewProtective factorPediatricsRJ1-570Type 2 immune response03 medical and health sciences0302 clinical medicineImmune systemSettore MED/38 - Pediatria Generale E Specialisticachildrenmedicine030212 general & internal medicineRisk factorAsthmaInnate immune systembusiness.industrySARS-CoV-2COVID-19asthmamedicine.diseaserespiratory tract diseases030228 respiratory systemInfectious disease (medical specialty)ImmunologyPediatrics Perinatology and Child HealthCytokine stormbusinessFrontiers in pediatrics
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Inhibition of Rac1 signaling by lovastatin protects against anthracycline-induced cardiac toxicity

2011

Normal tissue damage limits the efficacy of anticancer therapy. For anthracyclines, the clinically most relevant adverse effect is cardiotoxicity. The mechanisms involved are poorly understood and putative cardioprotectants are controversially discussed. Here, we show that the lipid-lowering drug lovastatin protects rat H9c2 cardiomyoblasts from doxorubicin in vitro. Protection by lovastatin is related to inhibition of the Ras-homologous GTPase Rac1. It rests on a reduced formation of DNA double-strand breaks, resulting from the inhibition of topoisomerase II by doxorubicin. Doxorubicin transport and reactive oxygen species are not involved. Protection by lovastatin was confirmed in vivo. I…

rac1 GTP-Binding ProteinCancer ResearchAnthracyclineDoxorubicin transportCardiac fibrosismedicine.medical_treatmentImmunologyPharmacologyBiologyDNA damage responsestatinsMiceCellular and Molecular NeuroscienceRho GTPasespolycyclic compoundsmedicineAnimalsDNA Breaks Double-StrandedMyocytes CardiacDoxorubicinLovastatinanthracyclinesCardiotoxicityAntibiotics AntineoplasticTroponin IConnective Tissue Growth FactorCell Biologymedicine.diseaseRatsCTGFDNA Topoisomerases Type IICytokinenormal tissue damageDoxorubicinOriginal Articlelipids (amino acids peptides and proteins)LovastatinAtrial Natriuretic FactorSignal Transductionmedicine.drugCell Death & Disease
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Is Saffron Able to Prevent the Dysregulation of Retinal Cytokines Induced by Ocular Hypertension in Mice?

2021

Cytokine- and chemokine-mediated signalling is involved in the neuroinflammatory process that leads to retinal ganglion cell (RGC) damage in glaucoma. Substances with anti-inflammatory properties could decrease these cytokines and chemokines and thus prevent RGC death. The authors of this study analysed the anti-inflammatory effect of a hydrophilic saffron extract standardized to 3% crocin content, focusing on the regulation of cytokine and chemokine production, in a mouse model of unilateral laser-induced ocular hypertension (OHT). We demonstrated that following saffron treatment, most of the concentration of proinflammatory cytokines (IL-1β, IFN-γ, TNF-α, and IL-17), anti-inflammatory cyt…

retinal glial cellsChemokinegenetic structuresmedicine.medical_treatmentNeurocienciasmicrogliasaffronInflammationPharmacologyArticleProinflammatory cytokineCrocinchemistry.chemical_compoundfractalkineNeurotrophic factorsMedicineFisiología animalbiologyMicrogliabusiness.industryRGeneral MedicineVEGFcytokineseye diseasescrocinVascular endothelial growth factorBDNFglaucomamedicine.anatomical_structureCytokinechemistrybiology.proteinocular hypertensionMedicineOftalmologíaOftalmología veterinariasense organsmedicine.symptombusinessJournal of clinical medicine
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Inflammatory cytokines shape a changing DNA methylome in monocytes mirroring disease activity in rheumatoid arthritis

2019

Objective: Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease that mainly targets joints. Monocytes and macrophages are critical in RA pathogenesis and contribute to inflammatory lesions. These extremely plastic cells respond to extracellular signals which cause epigenomic changes that define their pathogenic phenotype. Here, we interrogated how DNA methylation alterations in RA monocytes are determined by extracellular signals. Methods: High-throughput DNA methylation analyses of patients with RA and controls and in vitro cytokine stimulation were used to investigate the underlying mechanisms behind DNA methylation alterations in RA as well as their relationship with clinic…

rheumatoid arthritis0301 basic medicine*DAS28Immunology*disease activityGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineArthritis RheumatoidPathogenesisEpigenome03 medical and health sciences0302 clinical medicineRheumatologymedicineDAS28HumansImmunology and AllergyEpigenomics030203 arthritis & rheumatologyDNA methylationTumor Necrosis Factor-alphabusiness.industryMacrophagesMonocyteTNFaMethylationDNA Methylationmedicine.disease*rheumatoid arthritis030104 developmental biologymedicine.anatomical_structure*TNFaRheumatoid arthritis*DNA methylationImmunologyDNA methylationLeukocytes MononuclearCytokinesTumor necrosis factor alphaInflammation Mediatorsbusinessdisease activityBiomarkersAnnals of the Rheumatic Diseases
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Rho GTPases Are Involved in the Regulation of NF-κB by Genotoxic Stress

2001

A common cellular response to genotoxic agents and inflammatory cytokines is the activation of NF-kappaB. Here, we addressed the question of whether small GTPases of the Rho family are involved in the stimulation of NF-kappaB signaling by genotoxic agents or TNFalpha in HeLa cells. Inhibition of isoprenylation of Rho proteins by use of the HMG-CoA reductase inhibitor lovastatin attenuated UV-, doxorubicin-, and TNFalpha-induced degradation of IkappaBalpha as well as drug-stimulated DNA binding activity of NF-kappaB. Furthermore, NF-kappaB-regulated gene expression stimulated by either UV irradiation or treatment with TNFalpha was abrogated by lovastatin pretreatment. This indicates that iso…

rho GTP-Binding ProteinsBacterial ToxinsClostridium difficile toxin BGenotoxic StressGTPaseBiologyProinflammatory cytokinechemistry.chemical_compoundBacterial ProteinsNF-KappaB Inhibitor alphamedicineHumansLovastatinTumor Necrosis Factor-alphaNF-kappa BNF-kappa B p50 SubunitNF-κBCell BiologyCell biologyDNA-Binding ProteinsIκBαchemistryDoxorubicinI-kappa B ProteinsTumor necrosis factor alphaLovastatinHeLa CellsSignal Transductionmedicine.drugExperimental Cell Research
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Inhibition of small G proteins of the Rho family by statins orClostridium difficiletoxin B enhances cytokine-mediated induction of NO synthase II

2000

In order to investigate the involvement of Ras and/or Rho proteins in the induction of the inducible isoform of nitric oxide synthase (NOS II) we used HMG-CoA reductase inhibitors (statins) and Clostridium difficile toxin B (TcdB) as pharmacological tools. Statins indirectly inhibit small G proteins by preventing their essential farnesylation (Ras) and/or geranylgeranylation (Rho). In contrast, TcdB is a glucosyltransferase and inactivates Rho-proteins directly. Human A549/8- and DLD-1 cells as well as murine 3T3 fibroblasts were preincubated for 18 h with statins (1–100 μM) or TcdB (0.01–10 ng ml−1). Then NOS II expression was induced by cytokines. NOS II mRNA was measured after 4–8 h by R…

rho GTP-Binding ProteinsG proteinBacterial ToxinsMevalonic AcidNitric Oxide Synthase Type IISmall G ProteinClostridium difficile toxin BBiologyGene Expression Regulation EnzymologicMiceGeranylgeranylationBacterial ProteinsPolyisoprenyl PhosphatesPrenylationGTP-Binding ProteinsGene expressionAtorvastatinTumor Cells CulturedAnimalsHumansDrug InteractionsPyrrolesLovastatinPromoter Regions GeneticPharmacology3T3 CellsTransfectionMolecular biologyHeptanoic AcidsEnzyme InductionPapersCytokinesHydroxymethylglutaryl-CoA Reductase InhibitorsNitric Oxide SynthaseSignal transductionBritish Journal of Pharmacology
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Inhibition of Rho modulates cytokine-induced prostaglandin E2 formation in renal mesangial cells.

2003

Stimulation of rat mesangial cells for 24 h with interleukin-1β(IL-1β) plus forskolin (Fk) leads to a marked increase in prostaglandin E 2 (PGE 2 ) synthesis. This effect is further enhanced by the small G-protein Rho inhibitor toxin A. A similar increase in PGE 2 formation is obtained with Y27632, a Rho-dependent kinase inhibitor, and with lovastatin, a hydroxymethylglutaryl-coenzyme A inhibitor which depletes cells from geranylgeranyl moieties and thus blocks Rho activation. In parallel to the increased PGE 2 synthesis, a potentiation of IL-1β-induced secretory group IIA phospholipases A 2 (sPLA 2 -IIA) protein expression also occurs by Rho inhibition. However, only toxin A triggers an in…

rho GTP-Binding Proteinsmedicine.medical_treatmentBlotting WesternProstaglandinBiologyDinoprostonePhospholipases Achemistry.chemical_compoundmedicineAnimalsProstaglandin E2Molecular BiologyCells CulturedForskolinMesangial cellKinaseColforsinCell BiologyMolecular biologyGlomerular MesangiumRatsPhospholipases A2Cytokinechemistrylipids (amino acids peptides and proteins)Lovastatinmedicine.drugProstaglandin EInterleukin-1Biochimica et biophysica acta
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Modulation of salivary inflammatory markers and proteomic analysis in HNC and OSCC patients undergoing radiotherapy

2021

Head and neck cancer (HNC) includes malignant tumours that most commonly arise from the oral mucosa or lining of the head and neck regions. They are characterized according to their primary site of origin as malignancies of the nasal cavity and paranasal sinuses, pharynx, larynx, salivary glands and oral cavity. The majority of these neoplasms are epithelial tumours, among them the 90% are squamous cell carcinomas (SCC). HNC including the Oral Squamous cell carcinoma (OSCC), is the sixth most common neoplasia worldwide with an incidence estimated at 650,000 cases and 330,000 deaths per year. Despite all of the diagnostic and therapeutic advances, the 5-year survival rate remains relatively …

salivaproteomicsUNESCO::CIENCIAS MÉDICAShead and neck cancer:CIENCIAS MÉDICAS [UNESCO]cytokinesradiotherapy
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Consensus nomenclature for CD8(+) T cell phenotypes in cancer

2015

International audience; Whereas preclinical investigations and clinical studies have established that CD8+ T cells can profoundly affect cancer progression, the underlying mechanisms are still elusive. Challenging the prevalent view that the beneficial effect of CD8+ T cells in cancer is solely attributable to their cytotoxic activity, several reports have indicated that the ability of CD8+ T cells to promote tumor regression is dependent on their cytokine secretion profile and their ability to self-renew. Evidence has also shown that the tumor microenvironment can disarm CD8+ T cell immunity, leading to the emergence of dysfunctional CD8+ T cells. The existence of different types of CD8+ T…

senescenceT cellOncology and CarcinogenesisImmunology[SDV.CAN]Life Sciences [q-bio]/CancerBiologyCD8+ T cellsIFN gammaanergy03 medical and health sciencesstemness0302 clinical medicineImmune system[SDV.CAN] Life Sciences [q-bio]/Cancerexhaustionmedicine2.1 Biological and endogenous factorsImmunology and AllergyCytotoxic T cellAetiologyPoint of ViewCancer030304 developmental biologyCD8+ T cells; IFNγ; anergy; anticancer immunity; cytotoxicity; effector; exhaustion; senescence; stemness0303 health sciencesTumor microenvironmentCD8(+) T cellsCancermedicine.diseasePhenotype3. Good healthanticancer immunitymedicine.anatomical_structureeffectorOncologyImmunologycytotoxicityCytokine secretionCD8030215 immunologyIFNγ
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