Search Results - (Author, Cooperation:M. Neurath)
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1P. Shen ; T. Roch ; V. Lampropoulou ; R. A. O'Connor ; U. Stervbo ; E. Hilgenberg ; S. Ries ; V. D. Dang ; Y. Jaimes ; C. Daridon ; R. Li ; L. Jouneau ; P. Boudinot ; S. Wilantri ; I. Sakwa ; Y. Miyazaki ; M. D. Leech ; R. C. McPherson ; S. Wirtz ; M. Neurath ; K. Hoehlig ; E. Meinl ; A. Grutzkau ; J. R. Grun ; K. Horn ; A. A. Kuhl ; T. Dorner ; A. Bar-Or ; S. H. Kaufmann ; S. M. Anderton ; S. Fillatreau
Nature Publishing Group (NPG)
Published 2014Staff ViewPublication Date: 2014-02-28Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Animals ; Antigen-Presenting Cells/immunology/metabolism ; Antigens, CD40/immunology ; B-Lymphocytes/*immunology/*metabolism/secretion ; Encephalomyelitis, Autoimmune, Experimental/*immunology ; Female ; Humans ; Immunity/*immunology ; Interleukin-10/metabolism ; Interleukins/immunology/*metabolism/secretion ; Lymphocyte Activation ; Macrophages/cytology/immunology ; Male ; Mice ; Plasma Cells/immunology/metabolism ; Salmonella Infections/*immunology/microbiology ; T-Lymphocytes/immunology ; Toll-Like Receptor 4/immunologyPublished by: -
2Schlaak, J. F. ; Barreiros, A. P. ; Pettersson, S. ; Schirmacher, P. ; Meyer Zum Büschenfelde, K.-H. ; Neurath, M. F.
Oxford, UK : Blackwell Science Ltd
Published 2001Staff ViewISSN: 1365-3083Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: The aim of this study was to characterize the functional relevance of the transcription factor NF-κB in the pathogenesis of septic shock. BALB/c mice were infected with two wild-type (WT 1, WT 2) strains of S. typhimurium that induce NF-κB or an escape variant that lacks this ability (P21) at a dose of 1 × 109/animal, respectively. Furthermore, wild-type infected mice were treated with antisense oligonucleotides directed against NF-κB 24 h before and 3 or 6 h after infection, while mismatched oligonucleotides were used as controls. Subsequently, the clinical course, histological and immunological alterations were monitored. Infection with WT 1 and WT 2 strains led to lethal septic shock within 24–36 h. In contrast, infection with the P21 variant was not followed by fulminant septic shock. Treatment with specific antisense oligonucleotides against the p65 subunit of NF-κB 24 h before infection prevented the development of fulminant, lethal septic shock and was associated with a significant increase of survival. After 20 h, markedly depressed serum levels of interferon (IFN)-γ and interleukin (IL)-6 but not IL-10 and tumour necrosis factor (TNF)-α were observed in p65 antisense-treated compared to mismatched-treated animals. These data show that the ability of S. typhimurium to induce lethal septic shock is critically dependent on their capacity to induce NF-κB.Type of Medium: Electronic ResourceURL: -
3Goetz, M. ; Lehr, H. A. ; Neurath, M. F. ; Galle, P. R. ; Orth, T.
Oxford, UK : Blackwell Science Ltd
Published 2003Staff ViewISSN: 1365-3083Source: Blackwell Publishing Journal Backfiles 1879-2005Topics: MedicineNotes: Primary sclerosing cholangitis (PSC) is a chronic cholestatic disorder with a presumed autoimmune aetiopathogenesis. We have recently described a novel organ-specific rat model of fibrosing cholangitis induced by intrabiliary administration of the hapten-reagent 2,4,6-trinitrobenzenesulfonic acid (TNBS) with similarities to human PSC. In the present report, we have evaluated the long-term outcome of TNBS-induced cholangitis in this model. Mild stenosis of the common bile duct of female Lewis rats (n = 18) was achieved by subtotal ligation and cholangitis induced by TNBS injection (50 mg/kg) into the dilated bile duct after a second laparotomy. After 8 and 12 months, we found no evidence of cholangitis in serum chemistry or histology or retrograde cholangiography of TNBS-treated rats. Antineutrophil cytoplasmic antibodies were positive in 75% of animals but were not predictive of liver damage. Tumour necrosis factor-α levels were not elevated in serum or in mononuclear spleen cell supernatants. Our findings suggest that a single initial insult is not sufficient to trigger chronic progressive inflammation. Rather, perpetuation of inflammation probably requires additional stimuli.Type of Medium: Electronic ResourceURL: -
4Staff View
ISSN: 1433-0385Keywords: Key words: Crohn's disease – Ulcerative colitis – Mucosal immunology – Cytokines. ; Schlüsselwörter: Morbus Crohn – Colitis ulcerosa – mucosale Immunologie – Cytokine.Source: Springer Online Journal Archives 1860-2000Topics: MedicineDescription / Table of Contents: Zusammenfassung. Die chronisch entzündlichen Darmerkrankungen (CED: Morbus Crohn, Colitis ulcerosa) sind durch schubartig verlaufende destruierende Entzündungsreaktionen der Darmschleimhaut gekennzeichnet. In den letzten Jahren konnte gezeigt werden, daß bei diesen Erkrankungen eine pathologische Aktivierung des intestinalen Immunsystems durch mucosale Antigene auftritt. In der chronischen Phase der Erkankungen sowie bei der Entwicklung postoperativer Rezidive sind Änderungen in der Zellmigration sowie der Cytokinproduktion intestinaler Zellen wahrscheinlich von entscheidender Bedeutung. Basierend auf diesen neuen pathogenetischen Erkenntnissen werden zur Zeit innovative klinische Behandlungsstrategien getestet, die rekombinante antiinflammatorische Cytokine (IFN-α, IL-10, IL-11) und Inhibitoren von Adhäsionsmolekülen (ICAM), proinflammatorischen Cytokinen (TNF, IL-12) und deren Rezeptoren (TNF, IL-6R) umfassen.Notes: Summary. Inflammatory bowel diseases (IBD: Crohn's disease, ulcerative colitis) are chronic inflammatory and frequently relapsing diseases of the gut that ultimately lead to destruction of the intestinal tissue. Recent evidence suggests that a pathologic activation of the mucosal immune system in response to antigens is a key factor in the pathogenesis of IBD. Furthermore, changes in cell migration and cytokine production appear to contribute to the perpetuation of IBD and the postoperative recurrence of Crohn's disease. Based on recent advances in our understanding of the pathogenesis of IBD, several new therapeutic strategies are currently being tested in clinical practice, including recombinant anti-inflammatory cytokines (IFN-α, IL-10, IL-11) and inhibitors of cell adhesion molecules (ICAM), proinflammatory cytokines (TNF, IL-12) and their receptors (TNF, IL-6R).Type of Medium: Electronic ResourceURL: -
5Staff View
ISSN: 1432-1262Keywords: Keywords Inflammatory bowel disease ; Animal models ; CytokinesSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Abstract Inflammatory bowel diseases (IBDs) in humans are complex chronic inflammatory disorders of largely unknown cause. Several mouse models that in some respects resemble human IBDs have recently been developed and have provided new insights into immunoregulatory processes in the gut. Both genetic and environmental factors have been shown to be involved in chronic intestinal inflammation. In most of the models CD4+ T lymphocytes have been identified as central mediators of inflammation. Inappropriate activation of TH1-dominated cytokine pathways upon contact with luminal bacterial antigens and lack of tolerance appear to be crucial for intestinal pathology. We present a brief overview of important animal models of IBD and describe the recent progress in understanding the mechanisms that contribute to chronic intestinal inflammation. Furthermore, novel immunotherapeutic approaches derived from such animal models are discussed.Type of Medium: Electronic ResourceURL: -
6Staff View
ISSN: 1618-2650Source: Springer Online Journal Archives 1860-2000Topics: Chemistry and PharmacologyType of Medium: Electronic ResourceURL: