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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Schottelius, Arndt J. Zügel, Ulrich Döcke, Wolf-Dietrich Zollner, Thomas M. Röse, Lars Mengel, Anne Buchmann, Bernd Becker, Andreas Grütz, Gerald Naundorf, Sandra Friedrich, Anke Gaestel, Matthias Asadullah, Khusru |
| Description | Country affiliation: Germany Author Affiliation: Schottelius AJ ( Bayer Schering Pharma AG, Berlin, Germany.) |
| Abstract | Mitogen-activated protein kinase-activated protein kinase 2 (MK2) is a downstream molecule of p38, involved in the production of TNF-alpha, a key cytokine, and an established drug target for many inflammatory diseases. We investigated the role of MK2 in skin inflammation to determine its drug target potential. MK2 deficiency significantly decreased plasma TNF-alpha levels after systemic endotoxin application. Deficient mice showed decreased skin edema formation in chronic 2-O-tetradecanoylphorbol-13-acetate (TPA)-induced irritative dermatitis and in subacute 2,4-dinitrofluorobenzene (DNFB)-induced contact hypersensitivity. Surprisingly, MK2 deficiency did not inhibit edema formation in subacute 2,4-dinitrochlorobenzene (DNCB)-induced contact allergy and even increased TNF-alpha and IL-1beta levels as well as granulocyte infiltration in diseased ears. Ear inflammation in this model, however, was inhibited by TNF-alpha neutralization as it was in the subacute DNFB model. MK2 deficiency also did not show anti-inflammatory effects in acute DNFB-induced contact hypersensitivity, whereas the p38 inhibitor, SB203580, ameliorated skin inflammation supporting a pathophysiological role of p38. When evaluating possible mechanisms, we found that TNF-alpha production in MK2-deficient spleen cells was strongly diminished after TLR stimulation but less affected after T-cell receptor stimulation. Our data suggest that MK2, in contrast to its downstream effector molecule, TNF-alpha, has a rather elusive role in T-cell-dependent cutaneous inflammation. |
| File Format | HTM / HTML |
| ISSN | 0022202X |
| e-ISSN | 15231747 |
| Journal | Journal of Investigative Dermatology |
| Issue Number | 2 |
| Volume Number | 130 |
| Language | English |
| Publisher | Elsevier |
| Publisher Date | 2010-02-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Dermatology Inflammation Intracellular Signaling Peptides And Proteins Metabolism Protein-serine-threonine Kinases Skin Pathology P38 Mitogen-activated Protein Kinases Animals Dermatitis, Contact Dinitrofluorobenzene Chemistry Granulocytes Cytology Homozygote Mice Mice, Inbred C57bl Receptors, Antigen, T-cell Enzymology Tetradecanoylphorbol Acetate Pharmacology Tumor Necrosis Factor-alpha |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology Dermatology |
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