Search results for "Complement C5"

showing 8 items of 18 documents

Vascular Leakage in Severe Dengue Virus Infections: A Potential Role for the Nonstructural Viral Protein NS1 and Complement

2006

Background Vascular leakage and shock are the major causes of death in patients with dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Thirty years ago, complement activation was proposed to be a key underlying event, but the cause of complement activation has remained unknown. Methods The major nonstructural dengue virus (DV) protein NS1 was tested for its capacity to activate human complement in its membrane-associated and soluble forms. Plasma samples from 163 patients with DV infection and from 19 patients with other febrile illnesses were prospectively analyzed for viral load and for levels of NS1 and complement-activation products. Blood and pleural fluids from 9 patient…

MaleAdolescentvirusesComplement C5aComplement Membrane Attack ComplexViral Nonstructural ProteinsDengue virusBiologyAntibodies Viralmedicine.disease_causeVirusCell LineDengue feverDenguemedicineHumansImmunology and AllergyAnaphylatoxinVascular DiseasesChildGlycoproteinsPleural Cavityvirus diseasesComplement System ProteinsDengue VirusViral Loadmedicine.diseaseVirologyComplement systemInfectious DiseasesCase-Control StudiesChild PreschoolImmunologybiology.proteinRNA ViralFemaleAntibodyComplement membrane attack complexViral loadThe Journal of Infectious Diseases
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Complement component deficiencies and infection: C5, C8 and C3 deficiencies in three families.

1992

Three families are described with complement component deficiencies. In one family, five children had C5 deficiency; in a second family, two children had C8 deficiency and one child in a third family had C3 deficiency. The index cases were identified during screening of patients with recurrent pyogenic infections, recurrent meningitis and meningococcaemia. Two of the five C5 deficient patients had recurrent meningitis and meningococcaemia, two had recurrent respiratory tract infections and otitis and one was healthy. One of the C8 deficient patients had meningitis, meningococcaemia and pneumonia, whereas his sibling with the same deficiency was healthy. The patient with C3 deficiency had fo…

MalePediatricsmedicine.medical_specialtyComplement Hemolytic Activity AssayMeningitis BacterialRecurrenceImmunopathologyRecurrent meningitisMedicineHumansSiblingChildRespiratory Tract Infectionsbusiness.industryMeningitis PneumococcalComplement C5Complement C3C5 Deficiencymedicine.diseaseComplement C8PedigreePneumoniaOtitisChild PreschoolPediatrics Perinatology and Child HealthImmunologyFemalemedicine.symptomComplicationbusinessMeningitisEuropean journal of pediatrics
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Chemotactic response of human alveolar macrophages and blood monocytes elicited by exposure to sulfur dioxide.

1996

An experimental study was undertaken to investigate the in vitro effect of sulfur dioxide on the chemotactic activity of alveolar macrophages (AM) and blood monocytes (BM). The cells were placed on a polycarbonate membrane and exposed to SO2 0.5, 1.5 and 2.5 ppm for 15 min. Control experiments were performed with exposure of the cells to synthetic air with 5% CO2. After gas exposure the cells were incubated with the chemotactic active agent C5a in 5% carbon dioxide (CO2) at 37 degrees C for 60 min. The numbers of AM and BM passing actively through the membrane were quantified using light microscopy. Our results show a dose-dependent reduction in the migration rate of cells under SO2 exposur…

MaleProgrammed cell deathComplement C5aIn Vitro Techniquescomplex mixturesMonocyteschemistry.chemical_compoundMacrophages AlveolarCytotoxic T cellHumansSulfur DioxideSulfur dioxideAgedAir PollutantsChemistryChemotaxisChemotaxisGeneral MedicineMiddle AgedMolecular biologyIn vitrorespiratory tract diseasesChemotaxis LeukocyteMembraneActive agentBiochemistryCarbon dioxideFemaleResearch in experimental medicine. Zeitschrift fur die gesamte experimentelle Medizin einschliesslich experimenteller Chirurgie
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Linking C5 deficiency to an exonic splicing enhancer mutation

2005

Abstract As an important component of the innate immune system, complement provides the initial response to prevent infections by pathogenic microorganisms. Patients with dysfunction of C5 display a propensity for severe recurrent infections. In this study, we present a patient with C5 deficiency demonstrated by immunochemical and functional analyses. Direct sequencing of all C5 exons displayed no mutation of obvious functional significance, except for an A to G transition in exon 10 predicting an exchange from lysine to arginine. This sequence alteration was present in only one allele of family members with a reduced serum C5 concentration and in both alleles of the patient with almost com…

MaleSequence analysisDNA Mutational AnalysisImmunologyExonic splicing enhancerBiologymedicine.disease_causeExonmedicineHumansImmunology and AllergyGeneFamily HealthGeneticsMutationSplice site mutationComplement C5ExonsSequence Analysis DNAC5 DeficiencyMolecular biologyAlternative SplicingPhenotypeChild PreschoolMutationRNA splicingThe Journal of Immunology
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Proteomic Profiling of Secreted Proteins for the Hematopoietic Support of Interleukin-Stimulated Human Umbilical Vein Endothelial Cells

2013

Human umbilical cord vein endothelial cells (HUVECs) secrete a number of factors that greatly impact the proliferation and differentiation of hematopoietic stem and progenitor cells (HSPCs). These factors remain largely unknown. Here, we report on the most comprehensive proteomic profiling of the HUVEC secretome and identified 827 different secreted proteins. Two hundred and thirty-one proteins were found in all conditions, whereas 369 proteins were identified only under proinflammatory conditions following IL-1β, IL-3, and IL-6 stimulation. Thirteen proteins including complement factor b (CFb) were identified only under IL-1β and IL-3 conditions and may potentially represent HSPC prolifer…

ProteomicsSpectrometry Mass Electrospray IonizationInterleukin-1betaBiomedical EngineeringComplement C5blcsh:MedicineAntigens CD34BiologyComplement factor BUmbilical veinProinflammatory cytokineHuman Umbilical Vein Endothelial CellsHumansProgenitor cellCell ProliferationTransplantationInterleukin-6lcsh:RAntibodies MonoclonalComputational BiologyInterleukinComplement System ProteinsCell BiologyFlow CytometryHematopoietic Stem CellsMolecular biologyUp-RegulationComplement systemHaematopoiesisElectrophoresis Polyacrylamide GelInterleukin-3Stem cellPeptidesCell Transplantation
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Effcts of Dextran Sulphate (Dxs) on Lymphocyte Localization in Complement-Deficient Mice: Evidence that the Fifth Component of Complement is not Impl…

1984

AbstractThe effects of subcutaneously or intraperitoneally administered dextran sulphate (DXS) (5nmg/kg) on the subseguent 1 h localization of intravenously injected radiolabelled lymph node cells was investigated in complement deficient mice which lack C5.DXS proved to be equally as potent in depressing cell localizzation in deficient as compared to normal mice. These findings. indicate that the terminal complement components are not, essential for DXS activity.

RatónLymphocyteImmunologyCellCell CommunicationBiologyToxicologyMicechemistry.chemical_compoundCell MovementmedicineAnimalsLymphocytesComplement ActivationLymph nodePharmacologyComplement component 5Dextran SulfateComplement C5DextransBiological activityMolecular biologymedicine.anatomical_structureDextranMechanism of actionchemistryImmunologyFemaleLymph Nodesmedicine.symptomJournal of Immunopharmacology
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Complement C5 but not C3 is expendable for tissue factor activation by cofactor-independent antiphospholipid antibodies

2018

The complement and coagulation cascades interact at multiple levels in thrombosis and inflammatory diseases. In venous thrombosis, complement factor 3 (C3) is crucial for platelet and tissue factor (TF) procoagulant activation dependent on protein disulfide isomerase (PDI). Furthermore, C5 selectively contributes to the exposure of leukocyte procoagulant phosphatidylserine (PS), which is a prerequisite for rapid activation of monocyte TF and fibrin formation in thrombosis. Here, we show that monoclonal cofactor-independent antiphospholipid antibodies (aPLs) rapidly activate TF on myelomonocytic cells. TF activation is blocked by PDI inhibitor and an anti-TF antibody interfering with PDI bin…

inorganic chemicals0301 basic medicineComplement factor I030204 cardiovascular system & hematologyMonocytesImmunoglobulin GThromboplastinThrombosis and HemostasisMice03 medical and health sciencesTissue factor0302 clinical medicineimmune system diseasesmedicineAnimalsPlateletneoplasmsBlood CoagulationMice KnockoutVenous ThrombosisComplement component 5biologyChemistryMonocyteComplement C5Complement C3Hematologynervous system diseasesbody regions030104 developmental biologymedicine.anatomical_structureCoagulationAntibodies Antiphospholipidbiology.proteinCancer researchAntibodyBlood Advances
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C5a complement and cytokine signaling mediate the pronociceptive effects of complex regional pain syndrome patient IgM in fracture mice.

2020

It has been proposed that complex regional pain syndrome (CRPS) is a posttraumatic autoimmune disease. Previously, we observed that B cells contribute to CRPS-like changes in a mouse tibia fracture model, and that early (12 months duration) CRPS patient IgM antibodies have pronociceptive effects in the skin and spinal cord of muMT fracture mice lacking B cells. The current study evaluated the pronociceptive effects of intraplantar or intrathecal injections of early CRPS IgM (5 µg) in muMT fracture mice. Skin and lumbar spinal cord were collected for immunohistochemistry and polymerase chain reaction analyses. Wild-type mice exhibited postfracture increases in complement component C5a and it…

medicine.medical_treatmentchemical and pharmacologic phenomenaComplement C5aArticleProinflammatory cytokine03 medical and health sciencesMice0302 clinical medicine030202 anesthesiologyMedicineAnimalsHumansSensitizationAutoimmune diseaseMicrogliabusiness.industryhemic and immune systemsrespiratory systemmedicine.diseaseSpinal cordMice Inbred C57BLDisease Models AnimalAnesthesiology and Pain MedicineNociceptionCytokineComplex regional pain syndromemedicine.anatomical_structureNeurologyImmunoglobulin MImmunologyCytokinesNeurology (clinical)business030217 neurology & neurosurgeryComplex Regional Pain SyndromesPain
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