Search results for " cytokine"

showing 10 items of 602 documents

Subclinical gut inflammation in ankylosing spondylitis

2015

Purpose of review Subclinical gut inflammation has been described in a significant proportion of patients with ankylosing spondylitis (AS), up to 10% of them developing it during the time of clinically overt inflammatory bowel disease. Histologic, immunologic, and intestinal microbiota alterations characterize the AS gut. Recent findings Microbial dysbiosis as well as alterations of innate immune responses have been demonstrated in the gut of AS. Furthermore, a growing body of evidence suggests that the gut of AS patients may be actively involved in the pathogenesis of AS through the production of proinflammatory cytokines, such as IL-23p19, and the differentiation of potentially pathogenic…

0301 basic medicineAnkylosing spondylitis; Gut inflammation; Innate lymphoid cells; Interleukin-17; Interleukin-23; Adaptive Immunity; Animals; Cytokines; Disease Models Animal; Dysbiosis; Gastrointestinal Microbiome; Humans; Immunity Innate; Inflammation; Inflammatory Bowel Diseases; Intestines; Macrophages; Mice; Spondylitis Ankylosing; Rheumatology; Medicine (all)MacrophageAdaptive ImmunityInterleukin-23Inflammatory bowel diseaseGastroenterologyMiceInterleukin 23InnateMedicineSubclinical infectionMedicine (all)Interleukin-17digestive oral and skin physiologyInnate lymphoid cellIntestineIntestinesCytokinesmedicine.symptomHumanAnkylosingmedicine.medical_specialtyDisease ModelInflammationdigestive system03 medical and health sciencesRheumatologyInternal medicineInnate lymphoid cellAnimalsHumansSpondylitis AnkylosingCytokineSpondylitisGut inflammationSpondylitiInflammationAnkylosing spondylitisAnimalbusiness.industryMacrophagesInflammatory Bowel DiseaseImmunityInflammatory Bowel Diseasesmedicine.diseaseImmunity InnateDysbiosiGastrointestinal MicrobiomeAnkylosing spondylitiDisease Models Animal030104 developmental biologyDysbiosisbusinessDysbiosisCurrent Opinion in Rheumatology
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Numerous Fasciola plasminogen-binding proteins may underlie blood-brain barrier leakage and explain neurological disorder complexity and heterogeneit…

2019

15 páginas, 5 figuras y 1 tabla

0301 basic medicineAntifibrinolyticContact systemmedicine.drug_classmedicine.medical_treatment030231 tropical medicineBradykininInflammationNeurological disorderFibrinolysis systemProteomic and mass spectrometry analysesBlood–brain barrierFasciola excretome/secretomeProinflammatory cytokine03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBlood-brain barrier leakageFibrinolysismedicineIndicators and preventionAcute and chronic phasesPlasminogen-binding proteinsFasciolabiologyHuman fascioliasis030108 mycology & parasitologymedicine.diseasebiology.organism_classificationInfectious Diseasesmedicine.anatomical_structurechemistryImmunologyAnimal Science and ZoologyParasitologymedicine.symptomNeurological disordersResearch Article
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H-ferritin and proinflammatory cytokines are increased in the bone marrow of patients affected by macrophage activation syndrome

2017

Summary Macrophage activation syndrome (MAS) is hyperinflammatory life-threatening syndrome, associated typically with high levels of serum ferritin. This is an iron storage protein including heavy (H) and light (L) subunits, categorized on their molecular weight. The H-/L subunits ratio may be different in tissues, depending on the specific tissue and pathophysiological status. In this study, we analysed the bone marrow (BM) biopsies of adult MAS patients to assess the presence of: (i) H-ferritin and L-ferritin; (ii) CD68+/H-ferritin+ and CD68+/L-ferritin+; and (iii) interleukin (IL)-1β, tumour necrosis factor (TNF) and interferon (IFN)-γ. We also explored possible correlations of these re…

0301 basic medicineBiopsymedicine.medical_treatment0302 clinical medicineBone MarrowcytokineImmunology and AllergyInterleukinBlood ProteinsSyndromeMiddle AgedC-Reactive ProteinCytokinemedicine.anatomical_structureCytokinesTumor necrosis factor alphaInflammation Mediatorsmedicine.symptommacrophage activation syndromeAdultImmunologyAntigens Differentiation MyelomonocyticInflammationmacrophageBiologyProinflammatory cytokine03 medical and health sciencesAntigens CDmedicineHumansAgedRetrospective StudiesInflammation030203 arthritis & rheumatologyMacrophagesferritinOriginal ArticlesMacrophage Activationmedicine.diseaseFerritinSettore MED/16 - Reumatologia030104 developmental biologyMacrophage activation syndromeApoferritinsImmunologybiology.proteinBone marrowCytokine; Ferritin; Hyperferritinaemic syndrome; Macrophage; Macrophage activation syndrome; Immunology and Allergy; Immunologycytokine; ferritin; hyperferritinaemic syndrome; macrophage; macrophage activation syndromehyperferritinaemic syndrome
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Abacavir induces platelet-endothelium interactions by interfering with purinergic signalling: A step from inflammation to thrombosis.

2017

The controversy connecting Abacavir (ABC) with cardiovascular disease has been fuelled by the lack of a credible mechanism of action. ABC shares structural similarities with endogenous purines, signalling molecules capable of triggering prothrombotic/proinflammatory programmes. Platelets are leading actors in the process of thrombosis. Our study addresses the effects of ABC on interactions between platelets and other vascular cells, while exploring the adhesion molecules implicated and the potential interference with the purinergic signalling pathway. The effects of ABC on platelet aggregation and platelet-endothelium interactions were evaluated, respectively, with an aggregometer and a flo…

0301 basic medicineBlood PlateletsEndotheliumPlatelet AggregationAnti-HIV AgentsInflammationPharmacologyBiologyProinflammatory cytokine03 medical and health sciences0302 clinical medicinePlatelet Adhesivenessplatelet-endothelium interactionsVirologymedicineHumansPlatelet030212 general & internal medicinePlatelet activationPharmacologyInflammationCell adhesion moleculePurinergic receptorDeoxyguanine NucleotidesThrombosisPurinergic signallingIntercellular Adhesion Molecule-1Platelet ActivationAbacavirNRTIsDideoxynucleosidesCell biologycardiovascular diseasesP-Selectin030104 developmental biologymedicine.anatomical_structureCardiovascular DiseasesPurinesEndothelium Vascularmedicine.symptomSignal TransductionAntiviral research
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IL-17A/F in Leishmania major-resistant C57BL/6 mice.

2019

Proinflammatory IL-17 plays an important role in various diseases and defence against extracellular microorganisms. Healing of leishmaniasis is promoted by Th1/Tc1 cells, whereas Th2/Treg are associated with worsened disease outcome. In addition, high expression of IL-17A in Leishmania-susceptible BALB/c and artificial overexpression of IL-17A in T cells in resistant C57BL/6 mice worsened disease outcome. Since C57BL/6 mice lacking only IL-17A exhibited no phenotype, and IL-17A and IL-17F share similar receptors, but differentially regulate chemokine secretion, we studied mice lacking both IL-17A and IL-17F (IL-17A/F-/- ) in infections with Leishmania major. Interestingly, lesion volumes an…

0301 basic medicineC57BL/6CD4-Positive T-LymphocytesMaleDermatologyBiochemistryProinflammatory cytokineLesion030207 dermatology & venereal diseases03 medical and health sciencesMice0302 clinical medicineTh2 CellsmedicineAnimalsSecretionLeishmania majorReceptorMolecular BiologyIntraepithelial LymphocytesLeishmaniasisCrosses GeneticLeishmaniaMice Inbred BALB CbiologyInterleukin-17Th1 Cellsbiology.organism_classificationPhenotypeMice Inbred C57BL030104 developmental biologyPhenotypeChemokine secretionImmunologyDisease ProgressionCytokinesFemalemedicine.symptomExperimental dermatology
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The route to solve the interplay between inflammation, angiogenesis and anti-cancer immune response.

2016

Even though the crucial role played by inflammation in cancer development and progression was first hypothesized by Rudolf Virchow at the beginning of the nineteenth century, only recently inflammation has been recognized as a hallmark of cancer. At present, the biology underlying the humoral and cellular immune-suppressive cancer-associated inflammatory microenvironment is an active area of preclinical and clinical investigation.1, 2 Indeed, the possibility to modulate the inflammatory/immune microenvironment, by either antagonizing the tumor-associated immune-suppression or by enhancing the pre-existing anti-cancer immune response in tumor tissues, is a promising therapeutic option for ca…

0301 basic medicineCancer ResearchBevacizumabAngiogenesisColorectal cancerImmunologyInflammationModels Biologicalimmune responseProinflammatory cytokineImmunomodulation03 medical and health sciencesCellular and Molecular Neuroscienceinflammation angiogenesis and anti-cancer immune response0302 clinical medicineImmune systemNeoplasmsmedicinecancerCytotoxic T cellAnimalsHumansangiogenesis and anti-cancer immune responseNeovascularization Pathologicbusiness.industryangiogenesiFOXP3Cell BiologyNews and Commentarymedicine.diseaseBevacizumab030104 developmental biologyinflammation030220 oncology & carcinogenesisImmunologymedicine.symptombusinessmedicine.drug
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2018

Abstract TNFα is a prominent proinflammatory cytokine and a critical mediator for the development of many types of cancer such as breast, colon, prostate, cervical, skin, liver, and chronic lymphocytic leukemia. Binding of TNFα to TNFR1 can lead to divergent signaling pathways promoting predominantly NF-κB activation but also cell death. We report here that the nitric oxide (NO) donor glyceryl trinitrate (GTN) converts TNFα, generated from immune cells or cancer cells stimulated by chemotherapy, into a prodeath mediator in colon and mammary cancer cells. GTN-mediated S-nitrosylation of cIAP1 on cysteines 571 and 574 inhibited its E3 ubiquitin ligase activity, which in turn reduced Lys63-lin…

0301 basic medicineCancer ResearchProgrammed cell deathbiologybusiness.industryCancerInflammationmedicine.diseaseUbiquitin ligaseProinflammatory cytokine03 medical and health sciences030104 developmental biologyImmune systemOncologyCancer cellbiology.proteinCancer researchmedicineTumor necrosis factor alphamedicine.symptombusinessCancer Research
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COVID-19: High-JAKing of the Inflammatory “Flight” by Ruxolitinib to Avoid the Cytokine Storm

2021

Since SARS-CoV-2 outbreak in December 2019, world health-system has been severely impacted with increased hospitalization, Intensive-Care-Unit (ICU) access and high mortality rates, mostly due to severe acute respiratory failure and multi-organ failure. Excessive and uncontrolled release of proinflammatory cytokines (cytokine release/storm syndrome, CRS) have been linked to the development of these events. The recent advancements of immunotherapy for the treatment of hematologic and solid tumors shed light on many of the molecular mechanisms underlying this phenomenon, thus rendering desirable a multidisciplinary approach to improve COVID-19 patients’ outcome. Indeed, currently available th…

0301 basic medicineCancer ResearchRuxolitinibruxolitinibmedicine.medical_treatmentlcsh:RC254-282Proinflammatory cytokine03 medical and health sciences0302 clinical medicineFibrosismedicineMyelofibrosisbusiness.industryferritinhyperinflammationCOVID-19Immunotherapylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.disease030104 developmental biologyCytokineOncologyJAK2030220 oncology & carcinogenesisImmunologyPerspectivebusinessJanus kinaseCytokine stormmedicine.drug
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Interleukin-6 increases expression of serine protease inhibitor Kazal type 1 through STAT3 in colorectal adenocarcinoma

2015

Inflammation promotes colorectal cancer (CRC) tumorigenesis, but the underlying molecular mechanisms are still being uncovered. Proinflammatory cytokine interleukin-6 (IL-6) stimulates survival signaling in CRC; inflammatory signals also regulate production and activity of proteases and their inhibitors. Over-expression of serine protease inhibitor Kazal type 1 (SPINK1) predicts an unfavorable outcome in colon cancer. The SPINK1 gene contains an IL-6 responsive element, suggesting it could act as an acute phase reactant. We assessed the connection between IL-6 and SPINK1, and the function and mechanism of this signaling. Our results show that Colo205 and HT-29 cells express and secrete SPIN…

0301 basic medicineCancer ResearchTumor microenvironmentProteasesStromal cellBiologymedicine.disease_cause3. Good healthProinflammatory cytokine03 medical and health sciencesParacrine signalling030104 developmental biology0302 clinical medicine030220 oncology & carcinogenesisCancer cellCancer researchbiology.proteinmedicineInterleukin 6CarcinogenesisMolecular BiologyMolecular Carcinogenesis
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Impact of glucocorticoids on systemic sirtuin 1 expression and activity in rats with adjuvant-induced arthritis

2020

The class III histone deacetylase sirtuin 1 (SIRT1) plays a pivotal role in numerous biological and physiological functions, including inflammation. An association between SIRT1 and proinflammatory cytokines might exist. In addition to their important role in inflammation associated with rheumatoid arthritis (RA), proinflammatory cytokines mediate the development of systemic effects. Here, we evaluated systemic SIRT1 expression and enzymatic activity, in peripheral blood mononuclear cells (PBMCs) and in liver isolated from rats with adjuvant-induced arthritis (AIA), treated or not with low or high doses of glucocorticoids (GCs). We also measured the production of tumour necrosis factor alph…

0301 basic medicineCancer Researchmedicine.medical_specialtyArthritisInflammationPeripheral blood mononuclear cellProinflammatory cytokine03 medical and health sciences0302 clinical medicineSirtuin 1Internal medicinemedicineAnimalsBeta (finance)Molecular BiologyGlucocorticoidsbiologySirtuin 1Brief ReportDNA Methylationmedicine.diseaseArthritis ExperimentalRats030104 developmental biologyEndocrinology030220 oncology & carcinogenesisRheumatoid arthritisbiology.proteinLeukocytes MononuclearCytokinesTumor necrosis factor alphamedicine.symptom
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