0000000000135043

AUTHOR

Wilhelm Schwaeble

0000-0001-8927-0864

showing 6 related works from this author

Expression of C1q, a subcomponent of the rat complement system, is dramatically enhanced in brains of rats with either Borna disease or experimental …

1995

In situ hybridization, RT-PCR and Northern blot analysis as well immunohistochemistry were used to examine the expression of C1q, a subcomponent of the rat complement system, in brains of rats infected with Borna disease virus (BDV) and rats afflicted with experimental allergic encephalomyelitis (EAE) induced by the adoptive transfer of myelin basic protein specific T cells. C1q mRNA, which was not detected in normal brain, became clearly detectable using RT-PCR analysis by d14 post infection (p.i.) with BDV. Maximal levels of C1q mRNA were reached 21 days p.i. when inflammatory reactions in the brain were also at a peak. Similarly, C1q mRNA was elevated when the clinical symptoms of EAE be…

Pathologymedicine.medical_specialtyAdoptive cell transferEncephalomyelitis Autoimmune ExperimentalEncephalomyelitisMolecular Sequence Datachemical and pharmacologic phenomenaIn situ hybridizationBiologyHippocampusPolymerase Chain Reactionimmune system diseasesGlial Fibrillary Acidic ProteinmedicineAnimalsNorthern blotRNA MessengerIn Situ HybridizationBrain ChemistryBorna diseaseMicrogliaBase SequenceComplement C1qRNA-Directed DNA Polymerasemedicine.diseaseBlotting NorthernImmunohistochemistryMyelin basic proteinComplement systemRatsUp-RegulationBlotting Southernmedicine.anatomical_structureNeurologyBorna Diseasebiology.proteinFemaleNeurology (clinical)MicrogliaJournal of the neurological sciences
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Expression of properdin in human monocytes

1994

Properdin is the only known positive regulator of the alternative pathway of complement activation. Northern blot analysis of cell lines derived from fibroblasts, B-cells, hepatoma cells, and cells of the monocyte-macrophage lineage revealed properdin expression only in the myelomonocytic cell line HL-60, in the monoblastic cell line U-937 and in the monocytic line Mono Mac 6. Culture of Mono Mac 6 cells for 24 h with phorbol 12-myristate 13-acetate, bacterial lipopolysaccharide and the cytokines interleukin-1 beta and tumour necrosis factor-alpha enhanced mRNA abundance, with the strongest effect (tenfold) being observed with the lipopolysaccharide. In contrast, recombinant interferon-gamm…

AdultLipopolysaccharidesLipopolysaccharidemedicine.medical_treatmentMolecular Sequence DataEnzyme-Linked Immunosorbent AssayBiologyurologic and male genital diseasesBiochemistryMonocytesCell LineInterferon-gammachemistry.chemical_compoundTumor Cells CulturedmedicineHumansRNA MessengerNorthern blotBase SequenceProperdinTumor Necrosis Factor-alphaMacrophagesMonocyteBlotting NorthernMolecular biologyRecombinant ProteinsComplement systemCytokinemedicine.anatomical_structurechemistryCell cultureImmunologyAlternative complement pathwayCytokinesTetradecanoylphorbol AcetateProperdinInterleukin-1European Journal of Biochemistry
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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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Complement C1q is dramatically up-regulated in brain microglia in response to transient global cerebral ischemia.

2000

Abstract Recent evidence suggests that the pathophysiology of neurodegenerative and inflammatory neurological diseases has a neuroimmunological component involving complement, an innate humoral immune defense system. The present study demonstrates the effects of experimentally induced global ischemia on the biosynthesis of C1q, the recognition subcomponent of the classical complement activation pathway, in the CNS. Using semiquantitative in situ hybridization, immunohistochemistry, and confocal laser scanning microscopy, a dramatic and widespread increase of C1q biosynthesis in rat brain microglia (but not in astrocytes or neurons) within 24 h after the ischemic insult was observed. A marke…

MaleImmunologyIschemiaInflammationIn situ hybridizationBiologySulfur RadioisotopesProinflammatory cytokineRNA ComplementaryCerebrospinal fluidDownregulation and upregulationmedicineImmunology and AllergyAnimalsTransient (computer programming)Rats WistarComplement C1qIn Situ HybridizationPharmacologyMicrogliaComplement C1qBrainRNA Probesmedicine.diseaseImmunohistochemistryCell biologyComplement systemRatsUp-Regulationmedicine.anatomical_structureIschemic Attack TransientImmunologyMicrogliamedicine.symptomNeuroscienceDigoxigeninJournal of immunology (Baltimore, Md. : 1950)
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De novo expression of intercellular adhesion molecule 1 (ICAM-1, CD54) in pancreas cancer.

1993

We examined the expression of intercellular--adhesion molecule-I (ICAM-I, CD54) in 6 surgically removed pancreatic tumors and 8 pancreatic tumor cell lines. Immunohistochemistry revealed a varying percentage of ICAM-I-positive pancreas tumor cells, while normal pancreatic tissue (except for slight reactivity of endothelial cells) was not stained. The presence of the ICAM-I molecule on the cell surface and the expression of ICAM-I mRNA were investigated for 8 different pancreatic tumor cell lines. Three of these (Capan-I, Capan-2, QGP-I) expressed ICAM-I constitutively. In 4 of the ICAM-I-negative pancreas cancer cell lines, it was possible to induce a remarkable expression of ICAM-I by incu…

Cancer ResearchPathologymedicine.medical_specialtyPancreatic diseaseCellMolecular Sequence DataBiologyProinflammatory cytokineImmunoenzyme TechniquesPancreatic tumorAntigens CDmedicineTumor Cells CulturedHumansRNA MessengerRNA NeoplasmBase SequenceCell adhesion moleculeCancermedicine.diseaseIntercellular Adhesion Molecule-1Molecular biologyPancreatic Neoplasmsmedicine.anatomical_structureOncologyCell culturePancreasCell Adhesion MoleculesInternational journal of cancer
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Differential expression of the murine mannose-binding lectins A and C in lymphoid and nonlymphoid organs and tissues.

2003

Abstract Mannose-binding lectin (MBL), a member of the collectin family, binds to carbohydrate structures on the surfaces of micro-organisms and may serve as a recognition molecule of the lectin pathway of complement activation. In rodents two forms, MBL-A and MBL-C, were described and shown to be products of two related, but uncoupled, genes. The liver is the main source of MBL biosynthesis. For rat MBL-A, expression has also been described in the kidney. Here we report that the two forms of murine MBL are differentially expressed in a number of nonhepatic tissues. Real-time RT-PCR revealed that the liver is the major site of expression for both MBL genes. Lower copy numbers were found in …

MaleLymphoid TissueImmunologyCollectinchemical and pharmacologic phenomenaIn situ hybridizationMannose-Binding LectinMiceIntestine SmallImmunology and AllergyAnimalsProtein IsoformsIn Situ HybridizationMannan-binding lectinMice Inbred BALB CInnate immune systembiologyLectinbacterial infections and mycosesAcquired immune systemMolecular biologyImmunohistochemistryComplement systemAnimals NewbornLiverOrgan SpecificityLectin pathwaybiology.proteinFemaleSpleenJournal of immunology (Baltimore, Md. : 1950)
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