Ilse Zündorf
Goethe University Frankfurt
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Featured researches published by Ilse Zündorf.
Biochemical Pharmacology | 2002
Dana Albert; Ilse Zündorf; Theo Dingermann; Walter E. Müller; Dieter Steinhilber; Oliver Werz
The acylphloroglucinol derivative hyperforin is the major lipophilic constituent in the herb Hypericum perforatum (St. Johns wort). The aim of the present study was to investigate if hyperforin as well as extracts of H. perforatum can suppresses the activities of 5-lipoxygenase (5-LO) and cyclooxygenases (COX), key enzymes in the formation of proinflammatory eicosanoids from arachidonic acid (AA). In freshly isolated human polymorphonuclear leukocytes stimulated with Ca(2+) ionophore A23187, hyperforin inhibited 5-LO product formation with IC(50) values of about 1-2 microM, in the absence or presence of exogenous AA (20 microM), respectively, being almost equipotent to the well-documented 5-LO inhibitor zileuton (IC(50) = 0.5-1 microM). Experiments with purified human 5-LO demonstrate that hyperforin is a direct 5-LO inhibitor (IC(50) approximately 90 nM), acting in an uncompetitive fashion. In thrombin- or ionophore-stimulated human platelets, hyperforin suppressed COX-1 product (12(S)-hydroxyheptadecatrienoic acid) formation with an IC(50) of 0.3 and 3 microM, respectively, being about 3- to 18-fold more potent than aspirin. At similar concentrations, hyperforin suppressed COX-1 activity in platelets in presence of exogenous AA (20 microM) as well as in cell-free systems. Hyperforin could not interfere with COX-2 product formation and did not significantly inhibit 12- or 15-LO in platelets or leukocytes, respectively. We conclude that hyperforin acts as a dual inhibitor of 5-LO and COX-1 in intact cells as well as on the catalytic activity of the crude enzymes, suggesting therapeutic potential in inflammatory and allergic diseases connected to eicosanoids.
Mediators of Inflammation | 2014
Robert Fürst; Ilse Zündorf
Many diseases have been described to be associated with inflammatory processes. The currently available anti-inflammatory drug therapy is often not successful or causes intolerable side effects. Thus, new anti-inflammatory substances are still urgently needed. Plants were the first source of remedies in the history of mankind. Since their chemical characterization in the 19th century, herbal bioactive compounds have fueled drug development. Also, nowadays, new plant-derived agents continuously enrich our drug arsenal (e.g., vincristine, galantamine, and artemisinin). The number of new, pharmacologically active herbal ingredients, in particular that of anti-inflammatory compounds, rises continuously. The major obstacle in this field is the translation of preclinical knowledge into evidence-based clinical progress. Human trials of good quality are often missing or, when available, are frequently not suitable to really prove a therapeutical value. This minireview will summarize the current situation of 6 very prominent plant-derived anti-inflammatory compounds: curcumin, colchicine, resveratrol, capsaicin, epigallocatechin-3-gallate (EGCG), and quercetin. We will highlight their clinical potential and/or pinpoint an overestimation. Moreover, we will sum up the planned trials in order to provide insights into the inflammatory disorders that are hypothesized to be beneficially influenced by the compound.
PLOS ONE | 2009
Jörg Lucas; Annika Bilzer; Lorna Moll; Ilse Zündorf; Theodor Dingermann; Ludwig Eichinger; Oliver Siol; Thomas Winckler
The C-module-binding factor (CbfA) is a multidomain protein that belongs to the family of jumonji-type (JmjC) transcription regulators. In the social amoeba Dictyostelium discoideum, CbfA regulates gene expression during the unicellular growth phase and multicellular development. CbfA and a related D. discoideum CbfA-like protein, CbfB, share a paralogous domain arrangement that includes the JmjC domain, presumably a chromatin-remodeling activity, and two zinc finger-like (ZF) motifs. On the other hand, the CbfA and CbfB proteins have completely different carboxy-terminal domains, suggesting that the plasticity of such domains may have contributed to the adaptation of the CbfA-like transcription factors to the rapid genome evolution in the dictyostelid clade. To support this hypothesis we performed DNA microarray and real-time RT-PCR measurements and found that CbfA regulates at least 160 genes during the vegetative growth of D. discoideum cells. Functional annotation of these genes revealed that CbfA predominantly controls the expression of gene products involved in housekeeping functions, such as carbohydrate, purine nucleoside/nucleotide, and amino acid metabolism. The CbfA protein displays two different mechanisms of gene regulation. The expression of one set of CbfA-dependent genes requires at least the JmjC/ZF domain of the CbfA protein and thus may depend on chromatin modulation. Regulation of the larger group of genes, however, does not depend on the entire CbfA protein and requires only the carboxy-terminal domain of CbfA (CbfA-CTD). An AT-hook motif located in CbfA-CTD, which is known to mediate DNA binding to A+T-rich sequences in vitro, contributed to CbfA-CTD-dependent gene regulatory functions in vivo.
Mycoses | 2017
Athanasios Tragiannidis; Ioannis Kyriakidis; Ilse Zündorf; Andreas H. Groll
Macromolecular immunosuppressive monoclonal antibodies and fusion proteins directed against molecules or cells involved in inflammation and immunity represent a recent and important addition to our therapeutic armamentarium. Tumor necrosis alpha (TNFα) is a cytokine involved in systemic inflammation and clinical utilization of its antagonists has revolutionized treatment of juvenile rheumatoid and psoriatic arthritis, ankylosing spondylitis, Crohns disease, ulcerative colitis, and plaque psoriasis. Clinical utility has also been demonstrated for use against steroid‐refractory graft‐vs‐host disease and other immune‐mediated conditions. Currently, five anti‐TNFα agents are approved by the European Medicines Agency (EMA), including the monoclonal anti‐TNF antibodies infliximab, adalimumab, golimumab and certolizumab pegol along with etanercept, a TNFα‐receptor/IgG‐Fc fusion protein. Theoretical considerations related to their mode of action and clinical observations suggest that opportunistic infectious complications should be seriously considered as possible adverse events of macromolecular immunosuppressants. The purpose of this review is to critically analyze the literature on invasive fungal infections (IFIs) occurring in association with TNFα inhibitors alone or in combination with other immunosuppressive agents, with a focus on pediatric patients, and to provide a framework of evaluating the risk for IFIs in this population.
Pharmazie in Unserer Zeit | 2008
Andrea Wolf; Jennifer Schaack; Louise Freikamp; Sascha Reutzel; Ilse Zündorf; Theo Dingermann
Verschiedene Krankheiten, wie Duchennesche Muskeldystrophie aber auch die im vorherigen Beitrag erwahnte Cystische Fibrose konnen durch einen Mutationstyp verursacht werden, der zu einem fruhzeitigen Abbruch der Proteinsynthese fuhrt. Ein neuer Wirkstoff mit dem Kurzel PTC124 konnte bei allen diesen verschiedenen Krankheiten abhilfe leisten.
Pharmazie in Unserer Zeit | 2001
Ilse Zündorf; Theo Dingermann
Heute sind praktisch ausschlieslich Humaninsuline fur die Versorgung insulinpflichtiger Diabetiker im Handel. Die Herstellung dieser Wirkstoffe erfolgt biotechnisch bzw. gentechnisch. In dieser kurzen Ubersicht sollen die Besonderheiten verschiedener Verfahren erlautert werden, die letztlich alle den gleichen Wirkstoff liefern: Humaninsulin.
Planta Medica | 2017
Robert Fürst; Ilse Zündorf; Theo Dingermann
In the 19th century, cardio-active steroid glycosides, shortly cardiac glycosides, were scientifically established as drugs against heart failure. Their in vivo, cellular, and molecular actions as well as their predominant target, Na+-K+-ATPase, have been comprehensively investigated in the 20th century and the discovery of endogenous cardiac glycosides has fostered this research field. In the last years, however, results from clinical trials and meta-analyses have questioned their therapeutic value due to efficacy and safety issues. This has led to a considerable decline of their usage. Beyond the cardiovascular system, cardiac glycosides have been increasingly recognized as antitumor compounds and Na+-K+-ATPase has evolved into a promising drug target in oncology. A wealth of review articles exists that intensively discuss these topics. Surprisingly, the anti-inflammatory actions of cardiac glycosides, which were discovered in the 1960s, have so far hardly been perceived and have not yet been summarized. This review provides an overview of the in vivo and in vitro actions of cardiac glycosides on inflammatory processes and of the signaling mechanisms responsible for these effects: cardiac glycosides have been found to decrease inflammatory symptoms in different animal models of acute and chronic inflammation. Regarding the underlying mechanisms most research has focused on leukocytes. In these cells, cardiac glycosides primarily inhibit cell proliferation and the secretion of proinflammatory cytokines.
Pharmazie in Unserer Zeit | 2009
Ilse Zündorf; Theo Dingermann
2002 galten sie beim renommierten Wissenschaftsjournal Science als “Durchbruch des Jahres”, 2006 verhalfen sie den Forschern Andrew Z. Fire und Craig C. Mello zum Nobelpreis und jetzt postuliert eine kanadische Forschergruppe, dass die so oft gepriesene Wirksamkeit in verschiedenen, krankheitsrelevanten Tiermodellen nur aufgrund einer unspezifischen Stimulation des Immunsystems zustande gekommen ist.
Mycoses | 2017
Ioannis Kyriakidis; Athanasios Tragiannidis; Ilse Zündorf; Andreas H. Groll
An expanding list of immunomodulatory or immunosuppressive monoclonal antibodies (mAbs) and biologic therapeutics is currently entering clinical practice, particularly in the areas of oncology, transplantation and autoimmune disorders. These agents are directed against molecules or cells involved in inflammation and immunity and may therefore be associated with serious and opportunistic infections. The purpose of this review was to critically analyse the literature on invasive fungal infections (IFIs) occurring in association with mAbs and fusion proteins other than tumour necrosis alpha (TNF‐α) inhibitors, including therapeutics modulating T‐cell‐mediated pathologies (muromonab, abatacept, belatacept, ipilimumab, basiliximab, daclizumab), inducing lymphopenia (alemtuzumab), depleting CD20+ B cells (rituximab) and interfering with various targets (anakinra, natalizumab, blodalumab, ixekizumab and others) with a focus on children, and to provide a framework of evaluating the risk for IFIs in this population.
Deutsche Zeitschrift für Onkologie | 2014
Theo Dingermann; Ilse Zündorf
Patientinnen mit einem Ostrogenrezeptor- oder Progesteronrezeptor-exprimierendem Mammakarzinom erhalten in einem chemopraventiven Ansatz uber funf Jahre den Ostrogenrezeptorblocker Tamoxifen oder einen Aromatasehemmer. Sinn dieser Therapie ist es, eventuell verbliebene Tumorzellen daran zu hindern, Ostrogen-gesteuert weiter zu proliferieren. In der Praxis wird heute bei postmenopausalen Patientinnen meist eine sequenzielle Kombinationstherapie verordnet. Dabei wechseln die Patientinnen nach 2,5 Jahren Therapie mit Tamoxifen auf einen Aromatase-Inhibitor. Oder sie beginnen die Chemoprophylaxe mit einem Aromatase-Inhibitor und wechseln dann nach 2,5 Jahren auf Tamoxifen. Dieses sequenzielle Therapieschema wird auch deshalb empfohlen, da eine Tamoxifen-Therapie nicht bei jeder Patientin optimal wirksam zu sein scheint. Das kann daran liegen, dass Tamoxifen ein Prodrug ist, das vornehmlich uber das Cytochrom-P450-Isoenzym 2D6 (CYP2D6) zum aktiven Metaboliten umgewandelt werden muss. Dieses Enzym ist jedoch polymorph, d. h. es kommt auch in inaktiven Varianten vor. Dies lasst sich heute leicht durch einen Gentest aus Speichel oder Blut als Genomquelle bestimmen. Jedoch ist die Testung in Fachkreisen heftig umstritten.