Search results for "Complement C3"

showing 10 items of 69 documents

Secreted proteophosphoglycan of Leishmania mexicana amastigotes activates complement by triggering the mannan binding lectin pathway.

1997

Cutaneous lesions induced by infection of mice with the protozoan parasite, Leishmania mexicana, contain abundant amounts of a high molecular mass proteophosphoglycan (PPG), which is secreted by the amastigote stage residing in phagolysosomes of macrophages and can then be released into the tissue upon rupture of the infected cells. Amastigote PPG forms sausage-shaped but soluble particles and belongs to a novel class of serine-rich proteins that are extensively O-glycosylated by phosphooligosaccharides capped by mannooligosaccharides. The purified molecule is shown here to efficiently activate complement (C) and deplete hemolytic activity of normal serum and may prevent the opsonization of…

ImmunologyLeishmania mexicanaProtozoan ProteinsCollectinLeishmaniasis CutaneousLeishmania mexicanaMiceImmunology and AllergyAnimalsAmastigoteComplement ActivationMannan-binding lectinSerine proteaseMice KnockoutbiologyMacrophagesComplement C4Complement C3biology.organism_classificationCollectinsComplement systemAntibody opsonizationBiochemistryLectin pathwaybiology.proteinMice Inbred CBACalciumProteoglycansCarrier ProteinsEuropean journal of immunology
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Complement components in relation to macrophage function

1983

ImmunologyPharmacology toxicologyComplement C5aToxicologyComplement componentsOxygen ConsumptionPhagocytosisCell MovementAnimalsHumansMacrophagePharmacology (medical)PharmacologyChemistryMacrophagesComplement C5ThromboxanesComplement C3Complement System ProteinsReceptors ComplementComplement C3bImmunologyComplement C3aProstaglandinsLysosomesFunction (biology)Agents and Actions
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Alpha-1-antitrypsin-induced inhibition of complement-dependent phagocytosis.

1981

Abstract In a previous investigation, inhibition of complement-dependent rosette formation by alpha1-antitrypsin (α1-AT) was observed, and it was demonstrated that α1-AT interacts through its carbohydrate portion with C3 and its fragments. In the present study, the effect of α1-AT on the complement-receptor-mediated phagocytosis by human peripheral blood monocytes was examined. Purified α1-AT inhibited in a dose-dependent manner phagocytosis of C3-carrying yeast particles. Inhibition was selective, concerned only C3-receptor-mediated phagocytosis, neither Fc-receptor-mediated phagocytosis nor uptake of untreated yeast particles was blocked by α1-AT. It was demonstrated that α1-AT exerted it…

LeukemiaPhagocytosisImmunologyAlpha (ethology)Blood DonorsHematologyComplement receptorComplement C3Saccharomyces cerevisiaeCarbohydrateBiologyOpsonin ProteinsYeastPeripheral bloodMonocytesImmune systemBiochemistryPhagocytosisRosette formationalpha 1-AntitrypsinImmunology and AllergyHumansImmunobiology
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CiC3-1a-Mediated Chemotaxis in the Deuterostome Invertebrate Ciona intestinalis (Urochordata)

2003

Abstract Deuterostome invertebrates possess complement genes, and in limited instances complement-mediated functions have been reported in these organisms. However, the organization of the complement pathway(s), as well as the functions exerted by the cloned gene products, are largely unknown. To address the issue of the presence of an inflammatory pathway in ascidians, we expressed in Escherichia coli the fragment of Ciona intestinalis C3-1 corresponding to mammalian complement C3a (rCiC3-1a) and assessed its chemotactic activity on C. intestinalis hemocytes. We found that the migration of C. intestinalis hemocytes toward rCiC3-1a was dose dependent, peaking at 500 nM, and was specific for…

Lipopolysaccharidescomplement system ascidiansHemocytesMolecular Sequence DataIn situ hybridizationPertussis toxinimmunologyHemolymphEscherichia coliAnimalsImmunology and AllergyCiona intestinalisAmino Acid SequencePeptide sequenceinnate immunityInflammationCell-Free SystemChemotactic FactorsbiologyImmune SeraRiboprobeChemotaxisAnatomybiology.organism_classificationRecombinant ProteinsComplement systemCell biologyCiona intestinalisChemotaxis LeukocyteHemocyte migrationPertussis ToxinCell Migration InhibitionComplement C3a
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Refining Noninvasive Diagnostics In Nonalcoholic Fatty Liver Disease: Closing the Gap to Detect Advanced Fibrosis

2019

Liver Cirrhosismedicine.medical_specialtyHepatologybusiness.industryComplement C3medicine.diseaseGastroenterologyAdvanced fibrosisLiverNon-alcoholic Fatty Liver DiseaseInternal medicineNonalcoholic fatty liver diseasemedicineHumansClosing (morphology)businessAlgorithmsHepatology
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Stress proteins HSP90 and Gp96 in graft-versus-host disease : pathophysiological, diagnostic and therapeutic implication

2015

Allogeneic hematopoietic cell transplantation is a treatment for certain disorders including hematologic malignancies. Graft-versus-host-disease (GvHD) is a major, life-threatening complication. It is due to the recognition of recipient antigens by donor T cells, which activate and damage tissues. Intestinal barrier alteration plays a critical role in GvHD. Heat shock proteins (HSP)90 include five members, three cytosolic members named HSP90, and one member localized in endoplasmic reticulum (ER) called Gp96 and able to gain extracellular level in case of stress. We show in our thesis that 17AAG, a HSP90 inhibitor, reduces GvHD mortality in a mouse model. This effect is associated with an i…

Maladie du greffon contre l’hôte intestinale17AAG[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyIntestinal graft-versus-host disease[SDV.IMM] Life Sciences [q-bio]/ImmunologyMaladie du greffon contre l’hôteHSP90Complement C3Complément C3Gp96Graft-versus-host disease
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Moderate weight loss attenuates chronic endoplasmic reticulum stress and mitochondrial dysfunction in human obesity

2018

Abstract Objective In obese patients undergoing caloric restriction, there are several potential mechanisms involved in the improvement of metabolic outcomes. The present study further explores whether caloric restriction can modulate endoplasmic reticulum (ER) stress and mitochondrial function, as both are known to be mechanisms underlying inflammation and insulin resistance (IR) during obesity. Methods A total of 64 obese patients with BMI ≥35 kg/m2 underwent a dietary program consisting of 6 weeks of a very-low-calorie diet followed by 18 weeks of low-calorie diet. We evaluated changes in the metabolic and inflammatory markers -TNFα, hsCRP, complement component 3 (C3c), and retinol bindi…

Male0301 basic medicineGPX1MitochondrionSystemic inflammationmedicine.disease_causeGlutathione Peroxidase GPX10302 clinical medicineSirtuin 1Endoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsMembrane Potential MitochondrialbiologyComplement C3Middle AgedEndoplasmic Reticulum StressMitochondriaC-Reactive ProteinFemalemedicine.symptomAdultmedicine.medical_specialty030209 endocrinology & metabolism03 medical and health sciencesInsulin resistanceInternal medicineWeight LossmedicineHumansObesityMolecular BiologyCaloric RestrictionInflammationGlutathione PeroxidaseRetinol binding protein 4Tumor Necrosis Factor-alphabusiness.industryEndoplasmic reticulumCell Biologymedicine.disease030104 developmental biologyEndocrinologySpainbiology.proteinUnfolded protein responseInsulin ResistanceReactive Oxygen SpeciesbusinessRetinol-Binding Proteins PlasmaOxidative stressMolecular Metabolism
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Genetic control of C3 production by the S region of the mouse MHC.

1988

SUMMARY The present paper reports evidence indicating that the level of the third complement component (C3) is regulated by the S region of the murine H-2 complex. In fact, using congenic strains of mice we demonstrate that mice with the k haplotype at the S region show high C3 levels, whereas mice with the d haplotype at the S region show low C3 levels.

MaleGeneticsRatónImmunologyHaplotypeH-2 AntigensCongenicMice Inbred StrainsComplement C3ImmunogeneticsBiologyMajor histocompatibility complexHemolysisMajor Histocompatibility ComplexMiceGene Expression RegulationHaplotypesGeneticsbiology.proteinAnimalsAlleles
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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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Beneficial effects of C1 esterase inhibitor in ST-elevation myocardial infarction in patients who underwentsurgical reperfusion: a randomized double-…

2007

Background: The inflammatory cascade has been hypothesized to be an important mechanism of post-ischaemic myocardial reperfusion injury and several studies demonstrated that C1 esterase inhibitor (C1 -INH) is effective in post-ischaemia myocardial protection. Therefore, we aimed to investigate prospectively in a randomised double-blind study the cardioprotective effects of C1-INH in ST segment elevation myocardial infarction (STEMI) in patients who underwent emergent reperfusion with coronary artery bypass grafting (CABG). Methods: In this study, we enrolled 80 patients affected with STEMI who underwent emergent CABG. Patients were assigned in two groups (C1-INH group: receive 1000 Ul of C1…

MalePulmonary and Respiratory MedicineCardiac function curvemedicine.medical_specialtyMean arterial pressureCardiotonic AgentsMyocardial InfarctionCardiac indexMyocardial ReperfusionComplement C1 Inactivator ProteinsCoronary artery bypass surgeryReperfusion therapyDouble-Blind MethodInternal medicinemedicineHumansProspective StudiesMyocardial infarctionCoronary Artery BypassInfusions IntravenousSTEMI patients CABG C1 esterase inhibitor Reperfusion injury Complement cascade Myocardial function recoverybusiness.industryST elevationTroponin IComplement C4aGeneral MedicineMiddle Agedmedicine.diseaseMyocardial ContractionComplement Inactivating AgentsTreatment OutcomeComplement C3aCardiologyFemaleSurgeryCardiology and Cardiovascular MedicinebusinessReperfusion injury
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