Search results for "CHEMOKINE"

showing 10 items of 372 documents

Influence of HMB Supplementation and Resistance Training on Cytokine Response to Resistance Exercise

2014

The purpose of this study was to determine the effects of a multinutritional supplement including amino acids, β-hydroxy-β-methylbutyrate (HMB), and carbohydrates on cytokine responses to resistance exercise and training.Seventeen healthy, college-aged men were randomly assigned to a Muscle Armor™ (MA; Abbott Nutrition, Columbus, OH) or placebo supplement group and 12 weeks of resistance training. An acute resistance exercise protocol was administered at 0, 6, and 12 weeks of training. Venous blood samples at pre-, immediately post-, and 30-minutes postexercise were analyzed via bead multiplex immunoassay for 17 cytokines.After 12 weeks of training, the MA group exhibited decreased interfer…

Malemedicine.medical_specialtyStrength trainingmedicine.medical_treatmentInterleukin-1betaMedicine (miscellaneous)Immune functionGranulocytePlaceboBody Mass IndexInterferon-gammaYoung AdultDouble-Blind MethodMuscle damageInternal medicineMyokineMyokinemedicineDietary CarbohydratesValeratesHumansMicronutrientsAmino Acidsta315Chemokine CCL4Immune function; Muscle damage; Myokine; Nutrition; Strength trainingChemokine CCL2NutritionNutrition and DieteticsInterleukin-13business.industryInterleukin-6MonocyteBody WeightInterleukin-8InterleukinResistance TrainingVenous bloodHealthy VolunteersInterleukin-10Cytokinemedicine.anatomical_structureEndocrinologyNutrition AssessmentImmunologyDietary SupplementsCytokinesStrength trainingbusiness
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Enzymatically Degraded, Nonoxidized LDL Induces Human Vascular Smooth Muscle Cell Activation, Foam Cell Transformation, and Proliferation

2000

Background —Enzymatic, nonoxidative modification transforms LDL to an atherogenic molecule (E-LDL) that activates complement and macrophages and is present in early atherosclerotic lesions. Methods and Results —We report on the atherogenic effects of E-LDL on human vascular smooth muscle cells (SMC). E-LDL accumulated in these cells, and this was accompanied by selective induction of monocyte chemotactic protein-1 in the absence of effects on the expression of interleukin (IL)-8, RANTES, or monocyte inflammatory proteins-1α and -β). Furthermore, E-LDL stimulated the expression of gp130, the signal-transducing chain of the IL-6 receptor (IL-6R) family, and the secretion of IL-6. E-LDL invok…

Malemedicine.medical_specialtyVascular smooth muscleArteriosclerosismedicine.medical_treatmentBiologyFibroblast growth factorMuscle Smooth VascularStatistics NonparametricPhysiology (medical)Internal medicinemedicineHomeostasisHumansRNA MessengerAutocrine signallingAortaCells CulturedChemokine CCL2AgedFoam cellInterleukin-6Cell growthGrowth factorMonocyteCholesterol LDLReceptors Interleukin-6EnzymesCell biologymedicine.anatomical_structureEndocrinologyFemaleCardiology and Cardiovascular MedicineCell activationOxidation-ReductionCell DivisionFoam CellsCirculation
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Dynamics of CXC group chemokine platelet factor 4 (PF4) plasma levels in non-small cell lung cancer (NSCLC)

2012

CXC chemokines display pleiotropic effects participating not only in inflammation, but regulating angiogenesis and metastatic spread in cancer. Platelet factor 4 (PF4) is a 70-amino acid protein belonging to the CXC chemokine family. PF4 is also known as CXCL4. This chemokine is released from alpha-granules of activated platelets and binds with high affinity to heparin-like molecules promoting coagulation. Megakaryocytes respond to the presence of tumors by increasing their number in the bone marrow accompanied by increase in the number of platelets in circulation, causing changes in chemokine balance.

Medicine(all)ChemokinebiologyBiochemistry Genetics and Molecular Biology(all)Angiogenesisbusiness.industrylcsh:Rlcsh:MedicineCancerInflammationGeneral Medicinemedicine.diseaseGeneral Biochemistry Genetics and Molecular Biologymedicine.anatomical_structurePoster PresentationImmunologymedicinebiology.proteinPlateletPlatelet activationBone marrowmedicine.symptombusinessPlatelet factor 4Journal of Translational Medicine
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Influence of aging on murine neutrophil and macrophage function against Candida albicans.

2008

Previous work by our group showed that aged C57BL/6 mice develop an altered innate and adaptive immune response to Candida albicans and are more susceptible to systemic primary candidiasis. In this work, we used young (2-3 months old) and aged (18-20 months old) C57BL/6 mice to study in vitro the influence of aging on (1) the fungicidal activity of neutrophils and macrophages, (2) the production of cytokines by resident peritoneal macrophages in response to C. albicans, and (3) cell surface Toll-like receptor (TLR) 2 expression on resident peritoneal macrophages. Our results indicate that murine phagocytes have a fungicidal activity well preserved with aging. In vitro production of proinfla…

Microbiology (medical)ChemokineAgingNeutrophilsmedicine.medical_treatmentImmunologyBiologyMicrobiologyProinflammatory cytokineMicrobiologyMicePhagocytosisCandida albicansmedicineImmunology and AllergyMacrophageAnimalsCandida albicansCells CulturedInnate immune systemMicrobial ViabilityToll-Like ReceptorsGeneral Medicinebiology.organism_classificationCorpus albicansMice Inbred C57BLInfectious DiseasesCytokineImmunologybiology.proteinMacrophages PeritonealCytokinesTumor necrosis factor alphaFemaleFEMS immunology and medical microbiology
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IP-10 is an accurate biomarker for the diagnosis of tuberculosis in children.

2014

Summary Objective Performance of IFN-γ assays in children is compromised. Therefore, we investigated the utility of IP-10 for the detection of active tuberculosis (TB) and latent tuberculosis infection (LTBI) diagnosis in children; comparing its positivity with QuantiFERON-TB Gold In-Tube (QFN-G-IT) and T-SPOT.TB. Methods We studied 230 children from three groups: active TB, screening (healthy children without known exposure to active TB patient screened at school or by their paediatrician) and contact-tracing studies. IFN-γ release was determined by QFN-G-IT and T-SPOT.TB. IP-10 was detected in QFN-G-IT supernatants by ELISA. Results When combining QFN-G-IT and IP-10 assays, positive resul…

Microbiology (medical)Malemedicine.medical_specialtyTuberculosisAdolescentT-LymphocytesEnzyme-Linked Immunosorbent AssayInterferon-gammaLatent TuberculosisInternal medicineActive tbmedicineHumansTuberculosisSignificant riskChildRetrospective StudiesAntigens BacterialLatent tuberculosisbusiness.industryActive tuberculosismedicine.diseaseHealthy VolunteersChemokine CXCL10Infectious DiseasesChild PreschoolImmunologyBiomarker (medicine)CytokinesFemalebusinessBiomarkersThe Journal of infection
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Macrophage inflammatory protein-1.

2003

Macrophage inflammatory protein (MIP)-1alpha was identified 15 years ago as the first of now four members of the MIP-1 CC chemokine subfamily. These proteins termed CCL3 (MIP-1alpha), CCL4 (MIP-1beta), CCL9/10 (MIP-1delta), and CCL15 (MIP-1gamma) according to the revised nomenclature for chemokines are produced by many cells, particularly macrophages, dendritic cells, and lymphocytes. MIP-1 proteins, which act via G-protein-coupled cell surface receptors (CCR1, 3, 5), e.g. expressed by lymphocytes and monocytes/macrophages (MPhi), are best known for their chemotactic and proinflammatory effects but can also promote homoeostasis. The encouraging results of preclinical studies in murine model…

Molecular Sequence DataCCL18Cell BiologyBiologyMacrophage Inflammatory ProteinsCCL7BiochemistryCCL20CXCL2ImmunologyAnimalsHumansDiseaseCCL15Amino Acid SequenceCCL13CC chemokine receptorsChemokine CCL4Macrophage inflammatory proteinChemokine CCL3The international journal of biochemistrycell biology
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Importance of sarcopenia parameter changes after living donor liver transplantation

2017

The systemic role of muscle tissue is strengthened by the large system of hormones, chemokines and other mediators that constitute a dense network of communication between the skeletal muscle and the liver (1,2). This, associated with the evidence of a progressive malnutrition and depletion of muscle mass in end-stage liver disease (ESLD) patients, has led many to study the role of sarcopenia and its systemic effects in this setting, and to identify it as critical risk factor for post- liver transplantation (LT) mortality (3-5). Englesbe and colleagues found a direct correlation between central sarcopenia, measured by computerized tomography (CT), the total area of the psoas muscle (psoas a…

Muscle tissueChemokinePathologymedicine.medical_specialtybiologybusiness.industrySkeletal muscle030230 surgerymedicine.disease03 medical and health sciences0302 clinical medicinemedicine.anatomical_structureSarcopenia Liver TransplantationSarcopeniamedicinebiology.protein030211 gastroenterology & hepatologyLiving donor liver transplantationbusinessLetter to the EditorHormone
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Neuropeptide Y receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

2019

Neuropeptide Y (NPY) receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Neuropeptide Y Receptors [156]) are activated by the endogenous peptides neuropeptide Y, neuropeptide Y-(3-36), peptide YY, PYY-(3-36) and pancreatic polypeptide (PP). The receptor originally identified as the Y3 receptor has been identified as the CXCR4 chemokine recepter (originally named LESTR, [137]). The y6 receptor is a functional gene product in mouse, absent in rat, but contains a frame-shift mutation in primates producing a truncated non-functional gene [83]. Many of the agonists exhibit differing degrees of selectivity dependent on the species examined. For example, the potency of PP is greater…

MutationChemokinebiologyChemistryNeuropeptidePharmacologymedicine.disease_causeNeuropeptide Y receptorPeptide YYmedicinebiology.proteinPancreatic polypeptideReceptorPeptide sequenceIUPHAR/BPS Guide to Pharmacology CITE
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CXCR3-ligand-mediated skin inflammation in cutaneous lichenoid graft-versus-host disease.

2007

Background Lichenoid graft-versus-host disease (liGVHD) histologically shares several common features with other lichenoid dermatoses, such as cutaneous lupus erythematosus and lichen planus (LP), which collectively show a junctional infiltrate of cytotoxic lymphocytes with liquefaction of the basal layer ("interface dermatitis"). Because recent studies have shown a role for type I interferon (IFN)–associated inflammation, including lymphocyte recruitment via CXCR3 ligand interaction in cutaneous lupus erythematosus and LP, we hypothesized that similar mechanisms might also be involved in liGVHD. Methods Ten representative lesional skin biopsies taken from patients with different subsets of…

Myxovirus Resistance ProteinsChemokinePathologymedicine.medical_specialtyLichenoid EruptionsReceptors CXCR3CD3T-LymphocytesGraft vs Host DiseaseInflammationDermatitisDermatologyIn situ hybridizationCXCR3LigandsChemokine CXCL9Skin DiseasesGTP-Binding ProteinsMedicineCXCL10HumansLymphocytesRNA MessengerIn Situ Hybridizationbiologybusiness.industryLichen PlanusInterferon-alphaChemokine CXCL10stomatognathic diseasesImmunologyChronic DiseaseInterferon Type Ibiology.proteinCXCL9Immunohistochemistrymedicine.symptomEpidermisbusinessJournal of the American Academy of Dermatology
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Cancer cell–autonomous contribution of type I interferon signaling to the efficacy of chemotherapy

2014

International audience; The immune system is routinely confronted with cell death resulting from the physiological turnover of renewable tissues, as well as from pathological insults of several types. We hypothesize the existence of a mechanism that allows the immune system to discriminate between physiological and pathological instances of cell death, but the factors that determine whether cellular demise is perceived as a neutral, tolerogenic or immunogenic event remain unclear 1. Infectious insults are accompanied by so-called microbe-associated molecular patterns (MAMPs), i.e., viral or bacterial products that activate immune cells through a panel of pattern-recognition receptors (PRRs)…

Myxovirus Resistance ProteinsMessengerReceptor Interferon alpha-betaInbred C57BLchemotherapyInterferon alpha-betaMiceInterferonReceptorsAnthracyclinesNeoplasm MetastasisRIG-IPattern recognition receptorAdaptor ProteinsGeneral MedicineNeoadjuvant Therapy3. Good healthGene Expression Regulation NeoplasticTreatment OutcomeReceptors Pattern RecognitionInterferon Type I[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleImmunocompetencemedicine.drugReceptorSignal TransductionBreast Neoplasms[SDV.CAN]Life Sciences [q-bio]/CancerBiologyPattern RecognitionSettore BIO/09General Biochemistry Genetics and Molecular BiologyParacrine signallingImmune systemmedicineCXCL10AnimalsHumanscancerRNA MessengerAutocrine signallingNeoplastic[SDV.IMM.IMM]Life Sciences [q-bio]/Immunology/ImmunotherapyToll-Like Receptor 3Mice Inbred C57BLVesicular TransportChemokine CXCL10Adaptor Proteins Vesicular TransportGene Expression RegulationDoxorubicinImmunologyTLR3RNAAdaptor Proteins Vesicular Transport; Animals; Anthracyclines; Breast Neoplasms; Chemokine CXCL10; Doxorubicin; Female; Gene Expression Regulation Neoplastic; Humans; Immunocompetence; Interferon Type I; Mice Inbred C57BL; Myxovirus Resistance Proteins; Neoadjuvant Therapy; Neoplasm Metastasis; RNA; RNA Messenger; Receptor Interferon alpha-beta; Receptors Pattern Recognition; Toll-Like Receptor 3; Treatment Outcome; Signal Transduction
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