Harald Loppnow

ORCID: 0000-0003-0297-3327
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About
Contact & Profiles
Research Areas
  • Immune Response and Inflammation
  • Atherosclerosis and Cardiovascular Diseases
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Cell Adhesion Molecules Research
  • Sepsis Diagnosis and Treatment
  • Mechanical Circulatory Support Devices
  • Immune Cell Function and Interaction
  • Adipokines, Inflammation, and Metabolic Diseases
  • Lipid Membrane Structure and Behavior
  • Heart Failure Treatment and Management
  • Heart Rate Variability and Autonomic Control
  • Antimicrobial Peptides and Activities
  • Inflammasome and immune disorders
  • Cardiac Fibrosis and Remodeling
  • Immunotherapy and Immune Responses
  • RNA Interference and Gene Delivery
  • Cardiac Arrest and Resuscitation
  • Cytokine Signaling Pathways and Interactions
  • Fatty Acid Research and Health
  • Platelet Disorders and Treatments
  • Cardiac electrophysiology and arrhythmias
  • T-cell and B-cell Immunology
  • Cholesterol and Lipid Metabolism
  • Heart rate and cardiovascular health
  • T-cell and Retrovirus Studies

Martin Luther University Halle-Wittenberg
2010-2022

Luther University
2014

University Hospital in Halle
2010-2011

Max Planck Society
2010

Freie Universität Berlin
1991-2010

Institut für Hygiene und Umwelt
1963-2010

Japan Patent Office
2010

British Lung Foundation
2005

Friedrich Schiller University Jena
2005

Wittenberg University
2001

The cells that make up blood vessel walls appear to participate actively in local immune and inflammatory responses, as well certain vascular diseases. We tested here whether smooth muscle (SMC) can produce the important mediator IL6. Unstimulated SMC vitro elaborated 5 X 10(3) pg recIL6/24h (i.e., biological activity equivalent recombinant IL6 (recIL6), determined B9-assay with a recIL6 standard). Several pathophysiologically relevant factors augmented release from including 10 micrograms...

10.1172/jci114498 article EN Journal of Clinical Investigation 1990-03-01

Lipopolysaccharide (LPS) represents a major virulence factor of Gram‐negative bacteria (‘endotoxin’) that can cause septic shock in mammals including man. The lipid anchor LPS to the outer membrane, A, has peculiar chemical structure, harbours ‘endotoxic principle’ and is responsible for expression pathophysiological effects. Chemically modified A be endotoxically inactive, but may express strong antagonistic activity against LPS, property utilized antisepsis treatment. We show here these...

10.1046/j.1432-1327.2000.01204.x article EN European Journal of Biochemistry 2000-04-01

Objective: Multiple organ dysfunction syndrome (MODS) is the sequential failure of several systems after a trigger event, like sepsis or cardiogenic shock. Mortality rate high, up to 70%. Autonomic may substantially contribute development MODS. Our study aimed characterize a) spectrum autonomic critically ill MODS patients; b) whether different in patients receiving sedation, mechanical ventilation, catecholamines; c) age dependency MODS; and d) predicts mortality Design: Prospective cohort...

10.1097/01.ccm.0000178181.91250.99 article EN Critical Care Medicine 2005-09-01

Abstract Natural and synthetic lipid A as well natural oligosaccharide partial structures of LPS were examined in dose-response experiments to define the minimal structure necessary for IL-1 induction release cultures human mononuclear cells. Wild type (S. abortus equi) rough mutant was active minimal-doses 1 100 pg/ml, whereas heptaacyl hexaacyl (Salmonella minnesota Escherichia coli A, respectively) induced 1,000 pg/ml 10 respectively. Nanogram amounts (0.1 ng/ml) monodephospho E....

10.4049/jimmunol.142.9.3229 article EN The Journal of Immunology 1989-05-01

Many pathological effects of gram-negative bacteria are produced by their cell wall-derived lipopolysaccharides (LPSs). Differing pathogenicity LPSs, however, may depend on capacities to induce cytokines. Thus, we studied the lethal toxicity four nonenterobacterial LPSs and compared it with capacity mononuclear (MNC)-derived interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor (TNF). Unstimulated MNC did not release these LPS from phototrophic strain Rhodobacter capsulatus 37b4...

10.1128/iai.58.11.3743-3750.1990 article EN Infection and Immunity 1990-11-01

Abstract The activation of cells by endotoxin (LPS) is one the early host responses to infections with Gram-negative bacteria. lipid A part LPS molecules known represent endotoxic principle; however, specific requirements for expression biologic activity are still not fully understood. We previously found that a molecular conformation (endotoxic conformation) prerequisite be biologically active. In this study, we have investigated interdependence charge and natural chemically modified its...

10.4049/jimmunol.161.10.5464 article EN The Journal of Immunology 1998-11-15

Abstract The proinflammatory cytokine and potent chemoattractant IL-8 is involved in regulation of infectious or inflammatory processes. Human vascular endothelial cells (EC) smooth muscle (SMC) probably contribute to these responses by recognition and/or production rIL-8. We demonstrate here competitive binding studies with radiolabeled rIL-8 that EC fibroblasts, but not SMC, specifically bind low affinity. was saturated ligand concentrations up 80 nM 125I-rIL-8. Unlabeled...

10.4049/jimmunol.154.5.2375 article EN The Journal of Immunology 1995-03-01

Abstract Lipopolysaccharides (LPS) are well known inducers of interleukin 1 (IL1). Here we show that synthetic heptaacyl Salmonella minnesota (compound 516) and E. coli type 506) lipid A, as monodephospho part structures thereof, able to induce IL1 production in human mononuclear cells. The 4′‐monodephospho structure 505) was found be the most active inducer compared compound 506 1‐monodephospho 504). Synthetic A precursor Ia, lacking nonhydroxylated fatty acids 406), its 1‐ or (compounds...

10.1002/eji.1830161013 article EN European Journal of Immunology 1986-01-01

Inflammatory pathways are involved in the development of atherosclerosis. Interaction vessel wall cells and invading monocytes by cytokines may trigger local inflammatory processes. 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) standard medications used cardiovascular diseases. They thought to have anti-inflammatory capacities, addition their lipid-lowering effects. We investigated effect statins cytokine-mediated-interaction-model human vascular smooth muscle (SMC)...

10.1111/j.1582-4934.2010.01036.x article EN other-oa Journal of Cellular and Molecular Medicine 2010-02-16

During infection or inflammation, cells of the blood vessel wall, such as endothelial (EC) and smooth muscle (SMC), contribute to regulation immune response by production cytokines expression adhesion molecules. Little is known about mechanism(s) involved in stimulation vascular endotoxin (lipopolysaccharide [LPS]). As reported previously, LPS antagonists reduce LPS-induced cytokine vitro specifically, suggesting a specific recognition mechanism. We thus investigated role CD14 for SMC LPS....

10.1128/iai.63.3.1020-1026.1995 article EN Infection and Immunity 1995-03-01

Inflammation contributes to a variety of arterial diseases including atherosclerosis. Interleukin 1beta (IL-1beta) in its activated mature 17-kDa form may mediate aspects vascular inflammation. As shown previously, human wall cells, such as smooth muscle cells (SMC), express the IL-1beta precursor upon stimulation and IL-1beta-converting enzyme (ICE) constitutively but do not produce or ICE activity. How SMC, most numerous cell type arteries, release active has therefore remained perplexing...

10.1074/jbc.272.31.19569 article EN cc-by Journal of Biological Chemistry 1997-08-01

Abstract Interleukin‐7 (IL‐7) has long been known as a potent growth factor in lymphocyte development. However, recent data obtained vitro revealed additional functions for this cytokine, e.g. IL‐7 influences the generation of cytotoxic T cells and NK cells, higher concentrations, activates monocytes manner similar to bacterial lipopolysaccharide. Furthermore, human tonsillar B are able proliferate upon stimulation by cross‐linking cell receptor. Considering latter role proliferation, we...

10.1002/eji.1830261040 article EN European Journal of Immunology 1996-10-01
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