26rhk045 10.3205/26rhk045 urn:nbn:de:0183-26rhk0451 Meeting Abstract Frommer Frommer Klaus W. KW

Justus Liebig Universität Gießen, Abteilung für Rheumatologie und Klinische Immunologie, Campus Kerckhoff, Bad Nauheim, Deutschland

author Chakraborty Chakraborty Satabdi S

Justus Liebig Universität Gießen, Abteilung für Rheumatologie und Klinische Immunologie, Campus Kerckhoff, Bad Nauheim, Deutschland

author Rehart Rehart Stefan S

Agaplesion Markus-Krankenhaus, Klinik für Orthopädie und Unfallchirurgie, Bad Nauheim, Deutschland

author Müller-Ladner Müller-Ladner Ulf U

Justus Liebig Universität Gießen, Abteilung für Rheumatologie und Klinische Immunologie, Campus Kerckhoff, Bad Nauheim, Deutschland

author Neumann Neumann Elena E

Justus Liebig Universität Gießen, Abteilung für Rheumatologie und Klinische Immunologie, Campus Kerckhoff, Bad Nauheim, Deutschland

author German Medical Science GMS Publishing House

Düsseldorf

610 20260909 engl This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). M0656 045 Deutsche Gesellschaft für Rheumatologie Deutsche Gesellschaft für Orthopädische Rheumatologie Gesellschaft für Kinder- und Jugendrheumatologie 54. Kongress der Deutschen Gesellschaft für Rheumatologie und Klinische Immunologie (DGRh), 36. Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR), 40. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh) Deutscher Rheumatologiekongress 2026 Experimentelle & Translationale Rheumatologie Leipzig 20260909 20260912 ET.21 TextIntroduction: In rheumatoid arthritis (RA), the cytokines IL-1β, TNF-α and IFN-γ play a crucial role in the context of chronic joint inflammation and tissue destruction. Adipokines such as visfatin and metabolites such as lactate can also affect immune cells. The objective of this project was the analysis of potential interactions between cytokines, adipokines and metabolites regarding RA effector cells.Methods: Synovial fibroblasts (SF) and osteoblasts (OB) from RA patients were stimulated with visfatin, leptin and chemerin as well as lactic acid, lactate and succinate, each separately and in combination with IL-1β and TNF-α. RASF were stimulated with IL-1β, TNF-α and IFN-γ separately and with the combinations IL-1β+TNF-α and IL-1β+IFN-γ. Supernatants were analyzed for protein secretion using ELISA.Results: When combined with TNF-α, lactate lowered VEGF (-54% vs purely additive effect) and MMP3 (-63%) secretion by RASF, while the combination of lactic acid+IL-1β acted synergistically for VEGF (+48%). In contrast, IL-1β-induced IL-6 secretion was inhibited by lactate (-58%) and lactic acid (-50%). An interaction between adipokines and cytokines was partially observed for RASF: visfatin+IL-1β (+37%), leptin+IL-1β (-40%), chemerin+TNF-α (+45%). Interactions between IL-1β, TNF‑α and IFN-γ depended on the secreted factor: IL-1β+TNF-α showed a synergistic effect on IL-6 (+177%) in contrast to MCP-1 (+7%), for which there was practically no synergistic effect. In the case of IL-8 (+84%) and MMP3 (+206%), the combination of IL-1β+TNF-α caused a strong synergistic effect. The combination of IL-1β with IFN-γ in particular showed distinct differences in the resulting effects depending on the factor analyzed: a synergistic effect on IL-6 (+41%) and MCP-1 (+59%) in contrast to the antagonistic effect on IL-8 (-65%) and MMP3 (-81%).Conclusion: We observed differential interactions between cytokines in respect to their influence on the secretion profile of RASF. Interestingly, a cytokine may be proinflammatory on the one hand but also inhibit matrix destruction at the same time as could be see with IFN-g. The combination of adipokines and metabolites with cytokines used for treating RASF and RA-OB only lead to interactions in some but not all cases, suggesting that these factors can have effects on these cell types in vitro but only in specific combinations.Disclosures: Nothing to disclose. 0 0 0 0