gms | German Medical Science

42. Kongress der Deutschen Gesellschaft für Rheumatologie, 28. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie, 24. Wissenschaftliche Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie

17.-20. September 2014, Düsseldorf

Artikel

Artikel empfehlen

TH+ neuronal cell therapy in murine antigen-induced arthritis

Meeting Abstract

Suche in Medline nach

  • Matthias Ebbinghaus - Universitätsklinikum Jena, Institut für Physiologie I, Jena
  • Zsuzsa Jenei-Lanzl - Universitätsklinikum Regensburg, Klinik und Poliklinik für Innere Medizin I, Rheumatologie und Klinische Immunologie, Regensburg
  • Rainer H. Straub - University Hospital Regensburg, Lab. of Exp. Neuroendocrine Immunology and Rheumatology, Dept. of Internal Medicine, Regensburg
  • Hans-Georg Schaible - Universitätsklinikum Jena, Institut für Physiologie I, Jena

Deutsche Gesellschaft für Rheumatologie. Deutsche Gesellschaft für Orthopädische Rheumatologie. Gesellschaft für Kinder- und Jugendrheumatologie. 42. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh); 28. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh); 24. wissenschaftliche Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR). Düsseldorf, 17.-20.09.2014. Düsseldorf: German Medical Science GMS Publishing House; 2014. DocER.29

doi: 10.3205/14dgrh175, urn:nbn:de:0183-14dgrh1751

Veröffentlicht: 12. September 2014

© 2014 Ebbinghaus et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.

Gliederung

Text

Background: A long-lasting anti-inflammatory effect of generated catecholamine-producing tyrosine hydroxylase-positive (TH+) cells was recently shown in collagen type II-induced arthritis (CIA). The aim of this study was to investigate the importance of TH+ cells in another model of rheumatoid arthritis, in murine antigen-induced arthritis (AIA).

Methods: TH+ cells were generated from murine bone marrow-derived mesenchymal stem cells by specific catecholaminergic factors. AIA was induced in C57Bl/6 mice and one group of animals was treated by TH+ cell-transfer. Clinical signs of arthritis and pain were observed in all stages of inflammation. Furthermore the appearance of natural TH+ cells was determined immunohistologically.

Results: In contrast to CIA in DBA/1 mice, in our model only a small number of natural occurring TH+ cells were detectable. In acute AIA, natural TH+ cells were seen in the spleen but they disappeared in the chronic stage. After TH+ cell transfer, the severity of AIA was significantly reduced shortly after arthritis induction. In the follow-up, this anti-inflammatory effect diminished towards later phases of the disease. Surprisingly, after a second induction of AIA, short-term TH+ cell-mediated amelioration of joint swelling was observed again. Regarding pain, TH+ cell-treated mice showed less guarding and less reduction of withdrawal threshold for mechanical stimulation on the inflamed hind limb in acute AIA, indicating less hyperalgesia.

Conclusion: In AIA, anti-inflammatory effects of TH+ cells are related to the acute stage of inflammation. This demonstrates some differences between the CIA model and the antigen-induced monarthritic model. This demonstrates different ways of neuroimmune interactions in experimental arthritis.