Stähli, Alexandra BeatriceAlexandra BeatriceStähliScherler, CarinaCarinaScherlerZappalà, GrazianoGrazianoZappalàSculean, AntonAntonSculeanEick, SigrunSigrunEick2024-10-112024-10-112022https://boris-portal.unibe.ch/handle/20.500.12422/87586Periodontitis patients suffering concomitantly from rheumatoid arthritis (RA) often present with less inflamed periodontal tissues due to the ongoing anti-rheumatic therapy. This in vitro study was aimed to analyze whether anti-inflammatory drugs used in the therapy of RA can modulate the release of IL-8 and IL-1β by professional and non-professional immune cells stimulated with microorganisms. Periodontal ligament (PDL) fibroblasts, monocytic MONO-MAC-6-cells, and gingival keratinocytes were exposed to ibuprofen, prednisolone, and methotrexate with and without lysates of Fusobacterium nucleatum or Candida albicans. Supernatants were obtained and the levels of interleukin(IL)-8 and IL-1β (only MONO-MAC-6) were quantified. The addition of F. nucleatum lysate resulted in the strongest release of proinflammatory cytokines by PDL fibroblast and MONO-MAC-6 cells, while the modification by the tested anti-rheumatic drugs was only minor. After stimulation of the MONO-MAC-cells with F. nucleatum, prednisolone increased the release of IL-8, whereas methotrexate decreased the level. Anti-inflammatory drugs increased the adherence of C. albicans to epithelial cells. In patients with RA, the reduction of the microbial load in subgingival biofilm (biofilm removal) is of major importance; however, the intake of inflammatory drugs may interfere with the inflammatory response.enanti-inflammatory drugs oral cells periodontitis proinflammatory cytokines rheumatoid arthritis600 - Technology::610 - Medicine & healtharticle10.48350/1730923611805110.3389/froh.2022.960732