Search results for "granulocyte"

showing 10 items of 244 documents

Capacity of Gentamicin-Treated Pseudomonas aeruginosa to Induce Granulocyte Locomotion

1982

In protection against an invading parasite the host’s granulocytes play an essential role. To exert their defense the phagocytes have to be attracted to the site of parasite invasion. We have shown that Pseudomonas aeruginosa ATCC 27853 and other clinical isolates of this species can induce granulocyte migration, either directly or via generation of chemotactic activity in serum [1].

Granulocyte migrationPseudomonas aeruginosaChemistryChemotaxisBoyden chamberGranulocytemedicine.disease_causeMicrobiologyMinimum inhibitory concentrationmedicine.anatomical_structuremedicineParasite hostingGentamicinmedicine.drug
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Stimulation of pancreas and gastric carcinoma cell growth by interleukin 3 and granulocyte-macrophage colony-stimulating factor.

1991

Hematopoietic growth factors have recently been well characterized by complementary DNA scloning. For human epidermal growth factor, granulocyte-macrophage colony-stimulating factor recombinant proteins have been expressed in Escherichia coli . To reduce the toxic side effects of chemotherapy on the bone marrow, recombinant human granulocyte-macrophage colony—stimulating factor and recombinant human interleukin 3 were applied to patients suffering of gastrointestinal cancers. To determine the influence of recombinant human granulocyte-macrophage colony—stimulating factor and recombinant human interleukin 3 on human pancreas and gastric cancer cell cells in vitro, a sensitive microculture te…

HepatologybiologyEpidermal Growth FactorCell growthGrowth factormedicine.medical_treatmentGastroenterologyGranulocyte-Macrophage Colony-Stimulating FactorPancreatic NeoplasmsMiceEpidermal growth factorCell cultureStomach NeoplasmsCancer researchmedicinebiology.proteinTumor Cells CulturedAnimalsGrowth factor receptor inhibitorInterleukin-3Epidermal growth factor receptorRNA MessengerA431 cellsCell DivisionInterleukin 3
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Immunohistological differential diagnosis of inflammatory colonic diseases.

1984

Immunohistological investigations were carried out on human colonic tissue from, I healthy mucosa, 2 slightly inflamed mucosa, 3 mucosa with ulcerative colitis, 4 mucosa with Crohn's colitis, using antibodies against immunoglobulins and complement components. All our antibodies, including F(ab')2 fragments, demonstrated a progressive increase of labelled cells from healthy mucosa through slightly inflamed mucosa to mucosa with ulcerative colitis, in contrast to a complete absence of labelled cells in cases of Crohn's disease. The results are discussed with regard to their pathogenesis and their clinical significance for the differentiation of ulcerative colitis and Crohn's colitis.

Immunoglobulin Amedicine.medical_specialtyPathologyHistologyComplement Activating EnzymesGastroenterologyPathology and Forensic MedicinePathogenesisDiagnosis DifferentialCrohn DiseaseInternal medicinemedicineHumansColitisCrohn's diseasebiologybusiness.industryHistocytochemistryComplement C1qImmunochemistryComplement C4General MedicineComplement C3medicine.diseaseColitisUlcerative colitisdigestive system diseasesImmunoglobulin AImmunoglobulin MImmunoglobulin Mbiology.proteinImmunohistochemistryColitis UlcerativeAntibodybusinessGranulocytesHistopathology
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Cross-Inhibition of Interferon-Induced Signals by GM-CSF Through a Block in Stat1 Activation

2007

We investigated the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) on biologic signals induced by interferon-alpha (IFN-alpha) and IFN-gamma. In hematopoietic cell lines, IFN-induced signaling was investigated by Western blotting, electrophoretic mobility shift assays (EMSA), flow cytometry, protein-tyrosine phosphatase (PTP) assays, and RT-PCR. GM-CSF inhibited IFN-alpha-induced and IFN-gamma-induced Stat1 tyrosine phosphorylation in a time-dependent manner. EMSA showed that GM-CSF inhibited IFN-alpha-induced and IFN-gamma-induced IFN-gamma activator sequence (GAS) binding activity. As a consequence, IFN-induced transcription of the early response gene, IFN-stimulated…

ImmunologyPhosphataseSuppressor of Cytokine Signaling ProteinsProtein tyrosine phosphataseBiologyCell Linechemistry.chemical_compoundVirologyGranulocyte Colony-Stimulating FactorHumansPhosphorylationHistocompatibility Antigens Class IGranulocyte-Macrophage Colony-Stimulating FactorTyrosine phosphorylationDNACell BiologyMolecular biologySTAT1 Transcription FactorIRF1chemistryTyrosine kinase 2PhosphorylationInterleukin-3InterferonsSignal transductionInterferon Regulatory Factor-1Signal TransductionTranscription FactorsProto-oncogene tyrosine-protein kinase SrcJournal of Interferon & Cytokine Research
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Induction of interferon regulatory factors, 2′‐5′ oligoadenylate synthetase, P68 kinase and RNase L in chronic myelogenous leukaemia cells and its re…

1996

The genes crucially determining the therapeutic response of chronic myelogenous leukaemia (CML) to interferon-alpha (IFN-alpha) are unknown. Recently, two independent IFN-alpha signalling pathways were identified: the classic pathway mediates induction of 2'-5' oligoadenylate synthetase (2-5 OAS), p68 kinase and IFN regulatory factor-2 (IRF-2), whereas the alternate pathway leads to activation of IFN regulatory factor-1 (IRF-1). We investigated whether deficient or imbalanced expression of components of these two pathways is associated with resistance of CML cells to antiproliferative action of IFN alpha/beta. Constitutive and IFN-induced transcript levels of IFN-dependent genes in mononucl…

Interferon Regulatory Factor 2T-LymphocytesCellular differentiationmedicine.medical_treatmentProtein Serine-Threonine KinaseseIF-2 KinaseLeukemia Myelogenous Chronic BCR-ABL PositiveEndoribonucleases2'5'-Oligoadenylate SynthetasemedicineHumansRNA MessengerTreatment FailureInterferon alfaEIF-2 kinasebiology2'-5'-OligoadenylateInterferon-alphaHematologyBlotting NorthernHematopoietic Stem CellsPhosphoproteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticRepressor ProteinsCytokineIRF1Cancer researchbiology.proteinInterferon Regulatory Factor-2GranulocytesInterferon Regulatory Factor-1Transcription Factorsmedicine.drugInterferon regulatory factorsBritish Journal of Haematology
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Granulocyte–Macrophage Colony-Stimulating Factor Is Essential for Normal Wound Healing

2006

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a multipotent growth factor, which plays an important role during the process of wound healing. In clinical settings it has occasionally been employed in the treatment of cutaneous wounds of diverse etiologies. In a previous study, we have shown the positive influence of GM-CSF on full thickness excisional wounds in transgenic mice overexpressing GM-CSF in the basal layer of the epidermis. Direct GM-CSF action as well as indirect processes through the induction of secondary cytokines were proposed to contribute towards the beneficial effects. In this study, we analyzed the process of wound healing in transgenic mice overexpressing…

KeratinocytesMaleGenetically modified mousePathologymedicine.medical_specialtyPulmonary Fibrosismedicine.medical_treatmentNeovascularization PhysiologicMice TransgenicDermatologyNeovascularizationMiceBasal (phylogenetics)FibrosismedicineAnimalsMolecular BiologyCell ProliferationWound HealingEpidermis (botany)business.industryGrowth factorGranulocyte-Macrophage Colony-Stimulating FactorCell BiologyGeneral Medicinemedicine.diseaseGranulocyte macrophage colony-stimulating factorGranulation TissueCancer researchFemalemedicine.symptomWound healingbusinessBiotechnologymedicine.drugJournal of Investigative Dermatology Symposium Proceedings
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Unsaturated Fatty Acids Drive Disintegrin and Metalloproteinase (ADAM)-dependent Cell Adhesion, Proliferation, and Migration by Modulating Membrane F…

2011

The disintegrin-metalloproteinases ADAM10 and ADAM17 mediate the release of several cell signaling molecules and cell adhesion molecules such as vascular endothelial cadherin or L-selectin affecting endothelial permeability and leukocyte transmigration. Dysregulation of ADAM activity may contribute to the pathogenesis of vascular diseases, but the mechanisms underlying the control of ADAM functions are still incompletely understood. Atherosclerosis is characterized by lipid plaque formation and local accumulation of unsaturated free fatty acids (FFA). Here, we show that unsaturated FFA increase ADAM-mediated substrate cleavage. We demonstrate that these alterations are not due to genuine ch…

KeratinocytesMembrane FluidityADAM10Lipid BilayersVascular permeabilityBiologyADAM17 ProteinBiochemistryCapillary PermeabilityADAM10 ProteinCell MovementMembrane fluidityCell AdhesionAnimalsHumansCell adhesionMolecular BiologyCell ProliferationCell adhesion moleculeCell growthFluorescence recovery after photobleachingEndothelial CellsMembrane ProteinsCell BiologyAtherosclerosisADAM ProteinsCell biologyLipoproteins LDLADAM ProteinsHEK293 CellsFatty Acids UnsaturatedCholesterol EstersRabbitsAmyloid Precursor Protein SecretasesGranulocytes
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Repeated courses of granulocyte colony-stimulating factor in amyotrophic lateral sclerosis: clinical and biological results from a prospective multic…

2011

Granulocyte colony-stimulating factor (G-CSF) induces a transient mobilization of hematopoietic progenitor cells from bone marrow to peripheral blood. Our aim was to evaluate safety of repeated courses of G-CSF in patients with amyotrophic lateral sclerosis (ALS), assessing disease progression and changes in chemokine and cytokine levels in serum and cerebrospinal fluid (CSF). Twenty-four ALS patients entered an open-label, multicenter trial in which four courses of G-CSF and mannitol were administered at 3-month intervals. Levels of G-CSF were increased after treatment in the serum and CSF. Few and transitory adverse events were observed. No significant reduction of the mean monthly decrea…

Keywords:amyotrophic lateral sclerosiclinical trialhematopoietic stem cellSettore MED/26 - Neurologiagranulocyte colony-stimulating factorneuroinflammation
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Effects of ultraviolet light on immune parameters of the roach

2000

Ultraviolet B radiation penetrates into water and can affect fish health and the immune system, as is the case with mammals. Teleost fish, the roach, were exposed to UVB irradiation in aquariums and a panel of immune parameters was determined. In addition to altered blood picture and respiratory burst by blood leukocytes, changes were noted also in major lymphatic organs. Respiratory burst and natural cytotoxicity activity of head kidney granulocytes and mitogen-activated proliferation of splenic lymphocytes were suppressed. Although mostly transitory, some parameters remained suppressed for the following 2 weeks. Ultraviolet A radiation had only minor effects. The stress induced by UVB may…

KidneyUltraviolet RaysFishesGeneral MedicineBiologyKidneyToxicologyUltraviolet A RadiationRespiratory burstLymphatic systemmedicine.anatomical_structureImmune systemImmune SystemImmunopathologyImmunologymedicineUltraviolet lightAnimalsHumansLymphocytesCytotoxicityHeadGranulocytesRespiratory BurstToxicology Letters
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Cellular visualization of tissue prokallikrein in human neutrophils and myelocytes

1999

The vasoactive peptides bradykinin and kallidin (lysyl-bradykinin) have been implicated in diapedesis, a cellular process by which neutrophils migrate through endothelial cell gap junctions. The kinin peptides are released from their precursor moiety, kininogen, by the specific action of endoproteinases, the kallikreins. Kininogens have been demonstrated on the surface of neutrophils, and the presence of a competent processing enzyme such as tissue prokallikrein in neutrophils has been postulated, but firm evidence for this is still lacking. We have raised antibodies to a synthetic peptide that is a sequence copy of the activation segment of human TK and demonstrated that the anti-peptide a…

KininogenKallidinTissue kallikreinHematologyIn situ hybridizationKallikreinKininBiologyGranulocyteMolecular biologychemistry.chemical_compoundmedicine.anatomical_structurechemistryZymogenmedicinecirculatory and respiratory physiologyBritish Journal of Haematology
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