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479 results on '"Stange, E F"'

3. Optimierung der konservativen (Nichtbiologika‑)Therapie bei chronisch-entzündlichen Darmerkrankungen

Author

Stange, E. F. and Herrlinger, K.

Abstract

In den Leitlinien der Deutschen Gesellschaft für Gastroenterologie, Verdauungs- und Stoffwechselkrankheiten (DGVS) zu den chronisch-entzündlichen Darmerkrankungen (CED) Morbus Crohn und Colitis ulcerosa hat das konservative Vorgehen mit Aminosalizylaten, Kortikosteroiden und klassischen Immunsuppressiva wie Thiopurinen und Methotrexat immer noch Vorrang vor dem frühen Einstieg mit sog. Biologika (antikörperbasierte Therapien). Dies ist nicht nur aus Kostengründen sinnvoll, sondern auch wegen des oft blanden Verlaufs beider Erkrankungen und der Möglichkeit einer frühen Therapieeskalation („accelerated step up“) bei kompliziertem Verlauf mit einer effektiven Immunsuppression zur Umgehung einer Steroidlangzeittherapie. Die Ausschöpfung der konservativen Medikamente vermeidet auch die frühe Einschränkung der therapeutischen Optionen durch den nahezu regelhaften Wirkverlust und dann notwendigen Wechsel der wenigen zugelassenen Antikörper.

Published
2024
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4. Reduced Paneth cell alpha-defensins in ileal Crohn's disease

Author

Wehkamp, J, Salzman, N H, Porter, E, Nuding, S, Weichenthal, M, Petras, R E, Shen, B, Schaeffeler, E, Schwab, M, Linzmeier, R, Feathers, R W, Chu, H T, Lima, H, Fellermann, K, Ganz, T, Stange, E F, and Bevins, Charles L

Subjects
innate immunity, intestine, bacteria, inflammatory bowel disease
Abstract

The pathogenesis of Crohn's disease (CD), an idiopathic inflammatory bowel disease, is attributed, in part, to intestinal bacteria that may initiate and perpetuate mucosal inflammation in genetically susceptible individuals. Paneth cells (PC) are the major source of antimicrobial peptides in the small intestine, including human alpha-defensins HD5 and HD6. We tested the hypothesis that reduced expression of PC alpha-defensins compromises mucosal host defenses and predisposes patients to CD of the ileum. We report that patients with CID of the ileum have reduced antibacterial activity in their intestinal mucosal extracts. These specimens also showed decreased expression of PC alpha-defensins, whereas the expression of eight other PC products either remained unchanged or increased when compared with controls. The specific decrease of alpha-defensins was independent of the degree of inflammation in the specimens and was not observed in either CD of the colon, ulcerative colitis, or pouchitis. The functional consequence of alpha-defensin expression levels was examined by using a transgenic mouse model, where we found changes in HD5 expression levels, comparable to those observed in CD, had a pronounced impact on the luminal microbiota. Thus, the specific deficiency of PC defensins that characterizes ileal CD may compromise innate immune defenses of the ileal mucosa and initiate and/or perpetuate this disease.

Published
2005

5. NF-kappa B- and AP-1-mediated induction of human beta defensin-2 in intestinal epithelial cells by Escherichia coli Nissle 1917: A novel effect of a probiotic bacterium

Author

Wehkamp, Jan, Harder, J, Wehkamp, K, Wehkamp-von Meissner, B, Schlee, M, Enders, C, Sonnenborn, U, Nuding, S, Bengmark, S, Fellermann, K, Schroder, J M, and Stange, E F

Subjects
probiotic bacteria, human beta defensin 2 (HBD2), defensins, intestinal epithelial cells
Abstract

Little is known about the defensive mechanisms induced in epithelial cells by pathogenic versus probiotic bacteria. The aim of our study was to compare probiotic bacterial strains such as Escherichia coli Nissle 1917 with nonprobiotic, pathogenic and nonpathogenic bacteria with respect to innate defense mechanisms in the intestinal mucosal cell. Here we report that E. coli strain Nissle 1917 and a variety of other probiotic bacteria, including lactobacilli-in contrast to more than 40 different E. coli strains tested-strongly induce the expression of the antimicrobial peptide human beta-defensin-2 (hBD-2) in Caco-2 intestinal epithelial cells in a time- and dose-dependent manner. Induction of hBD-2 through E. coli Nissle 1917 was further confirmed by activation of the hBD-2 promoter and detection of the hBD-2 peptide in the culture supernatants of E. coli Nissle 1917-treated Caco-2 cells. Luciferase gene reporter analyses and site-directed mutagenesis experiments demonstrated that functional binding sites for NF-kappaB and AP-1 in the hBD-2 promoter are required for induction of hBD-2 through E. coli Nissle 1917. Treatment with the NF-kappaB inhibitor Helenalin, as well as with SP600125, a selective inhibitor of c-Jun N-terminal kinase, blocked hBD-2 induction by E. coli Nissle 1917 in Caco-2 cells. SB 202190, a specific p38 mitogen-activated protein kinase inhibitor, and PD 98059, a selective inhibitor of extracellular signal-regulated kinase 1/2, were ineffective. This report demonstrates that probiotic bacteria may stimulate the intestinal innate defense through the upregulation of inducible antimicrobial peptides such as hBD-2. The induction of hBD-2 may contribute to an enhanced mucosal barrier to the luminal bacteria.

Published
2004

21. Clarification

Author

Wehkamp, J, Bevins, C L, and Stange, E F

Published
2009

48. Stoffwechsel

Author

Ditschuneit, H. H., Scheuermann, E., Ditschuneit, H., Karoff, Ch., Zidek, W., Losse, H., Vetter, H., Schneider, A. G., Theurer, A., Stange, E. F., Heitz, J., Meyer-Sabellek, W., Arntz, H. R., Schulte, K. L., Gotzen, R., von Bergmann, K., Streicher, U., Leiß, O., Jensen, C., Gugler, R., Schneider, J., Kaffarnik, H., Zöfel, P., Klimt, F., Riesen, W., Mordasini, R., Wagner, H., Creutzfeldt, C., Cremer, P., Creutzfeldt, W., Seidel, D., Windler, E., Preyer, S., Klose, G., Luley, C., Schwartzkopff, W., Klör, H. U., Krone, W., Müller-Wieland, D., Greten, H., Kather, H., Bieger, W., Aktories, K., Wieland, E., Steinhardt, H. J., Paleos, G. A., Brandl, M., Fekl, W. L., Adibi, S. A., Pausch, J., Häussinger, D., Rasenack, J., Gerok, W., Käbisch, A., Hartenfels, S., Voegeli, R., Eberle, F., Gundlach, G., Pralle, H., Schweisfurth, H., Heinrich, J., Brugger, E., Schmidt, M., Löffler, W., Wingen, A.-M., Lemmen, C., Reiter, S., Banholzer, P., Gröbner, W., Miehlke, Klaus, editor, and Bergmann, J. F.

Published
1984
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49. Stoffwechsel I

Author

Diehm, C., Gnasso, A., Schettler, G., Augustin, J., Cremer, P., Wieland, H., Kreuzer, H., Seidel, D., Weisweiler, P., Merk, W., Schwandt, P., v. Hodenberg, E., Khoo, J. C., Vance, J., Witztum, J. L., Jensen, D., Steinberg, D., Stange, E. F., Spady, D. K., Dietschy, J. M., Miehlke, Klaus, editor, and Bergmann, J. F.

Published
1984
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