ACR Meeting Abstracts

ACR Meeting Abstracts

  • Home
  • Meetings Archive
    • ACR Convergence 2021
    • ACR Convergence 2020
    • 2020 ACR/ARP PRSYM
    • 2019 ACR/ARP Annual Meeting
    • 2018 ACR/ARHP Annual Meeting
    • 2017 ACR/ARHP Annual Meeting
    • 2017 ACR/ARHP PRSYM
    • 2016-2009 Meetings
    • Download Abstracts
  • Keyword Index
  • Advanced Search
  • Your Favorites
    • Favorites
    • Login
    • View and print all favorites
    • Clear all your favorites
  • Meeting Resource Center

Abstract Number: 1163

The Receptor For Advanced Glycation End Products (RAGE) As a Modulator Of Inflammatory Responses and Its Contribution To Gender-Specific Effects During Arthritis

Timo Wirth1, Christoph Kessel1, Philipp Becker2, Toni Weinhage3, Nadine Nippe4 and Dirk Foell5, 1Pediatric Rheumatology and Immunology, University of Muenster, Muenster, Germany, 2University of Muenster, Muenster, Germany, 3Pediatric Rheumatology and Immunology, University of Muenster, Münster, Germany, 4Department of Dermatology, University of Muenster, Münster, Germany, 5Department of Pediatric Rheumatology and Immunology, University of Muenster, Muenster, Germany

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Inflammation, inflammatory arthritis and innate immunity, Pathophysiology

  • Tweet
  • Email
  • Print
Session Information

Session Title: Innate Immunity and Rheumatic Disease

Session Type: Abstract Submissions (ACR)

Background/Purpose: The receptor for advanced glycation end products (RAGE) is a multi-ligand receptor expressed on various cells which interacts with a diverse class of ligands, e.g. ‘danger signals’ such as neutrophil-derived S100A12. RAGE has been implicated in the pathogenicity of various inflammatory diseases including inflammatory arthritis. However, the exact role of RAGE has not been sufficiently defined. Our recent data on S100A12-induced activation of monocytes points to a modulatory rather than pro-inflammatory function of human RAGE. To assess the role of RAGE in a more systematic way, we generated RAGE-/- mice and analyzed immune cell functions in vitro, followed by murine models of staphylococcus aureus infection (host defense), chemically induced colitis (mucosal immunity), lethal inflammatory liver injury (septic shock) and collagen induced arthritis (autoimmunity) comparing RAGE-/- and C57BL/6 wildtype (wt) mice.

Methods: Reactive oxygen species (ROS) production, phagocytosis and cytokine production of bone marrow derived monocytes were measured using flow cytometry. Staphylococcus aureus (S. aureus)infection was induced by footpad injection. Acute and chronic colitis were induced chemically by dextran sodium sulfate (DSS) solution. For the inflammatory liver injury model, mice were challenged with D-galactosamine (D-Gal) along with lipopolysaccharide (LPS). Arthritis was induced by injection of heterologous type II collagen (CII). 

Results: We observed no differences of cellular immune function (ROS and cytokine production, phagocytosis) in RAGE-/- compared to wt monocytes. Male, but not female RAGE-/- mice showed more footpad swelling and bacterial dissemination in the S. aureus infection model. In the DSS colitis model we observed no significant differences between the two strains, whereas RAGE-/- mice were significantly protected from lethal D‑Gal/LPS induced liver injury. RAGE-/- and wt mice develop arthritis at similar clinical scores and incidence with no significant differences in type II collagen autoantibody levels. However, in female animals there is a strong tendency towards aggravated disease, less remission and higher disease penetrance. 

Conclusion: Overall, the contribution of RAGE seems to largely depend on the disease model and cell type studied. While no overall differences with respect to immune cell activities were observed, a striking gender-specific effect of RAGE seems to be involved in some conditions, especially in arthritis. The exact role of RAGE and its soluble form (sRAGE) during the development of arthritis and the influence of gender-specific factors is under further investigation.


Disclosure:

T. Wirth,
None;

C. Kessel,
None;

P. Becker,
None;

T. Weinhage,
None;

N. Nippe,
None;

D. Foell,
None.

  • Tweet
  • Email
  • Print

« Back to 2013 ACR/ARHP Annual Meeting

ACR Meeting Abstracts - https://acrabstracts.org/abstract/the-receptor-for-advanced-glycation-end-products-rage-as-a-modulator-of-inflammatory-responses-and-its-contribution-to-gender-specific-effects-during-arthritis/

Advanced Search

Your Favorites

You can save and print a list of your favorite abstracts during your browser session by clicking the “Favorite” button at the bottom of any abstract. View your favorites »

ACR Pediatric Rheumatology Symposium 2020

© COPYRIGHT 2022 AMERICAN COLLEGE OF RHEUMATOLOGY

Wiley

  • Home
  • Meetings Archive
  • Advanced Search
  • Meeting Resource Center
  • Online Journal
  • Privacy Policy
  • Permissions Policies