Ursodeoxycholic acid attenuates the expression of proinflammatory cytokines in periodontal cells

Background Ursodeoxycholic acid (UDCA) is one of the first-line therapeutic medications used in treatment of cholestatic liver disease. Considering that periodontitis is epidemiologically linked to liver diseases, the question arises weather UDCA holds anti-inflammatory properties on periodontal health. Herein, we provide information that support anti-inflammatory effects of UDCA on three different periodontium-related cell types. Methods Gingival fibroblasts and the oral human squamous carcinoma cell line HSC-2 were exposed to interleukin (IL)1 beta and tumor necrosis factor (TNF)alpha with and without UDCA. Murine RAW 264.7 macrophages were incubated with sterile-filtered human saliva also in the presence of UDCA. The expression of inflammatory cytokines was measured by reverse transcription-polymerase chain reaction. Immunoassay was applied to detect the production of IL6. Immunostaining was performed for the p65 subunit to further support the anti-inflammatory role of UDCA. Results We report here that UDCA significantly reduced the IL1 beta and TNF alpha-induced expression of IL1, IL6, and IL8 in gingival fibroblasts and the HSC-2 cell line. In RAW 264.7 macrophages, UDCA attenuated the expression of IL1 alpha, IL1 beta, and IL6 that was increased by saliva. Immunoassay confirmed the capacity of UDCA to reduce inflammation-induced production of IL6 in gingival fibroblasts, HSC-2 and RAW 264.7 cells. Immunostaining revealed the blocking of nuclear translocation of p65 in gingival fibroblasts. Conclusions Taken together, UDCA can attenuate the provoked expression of pro-inflammatory cytokines in oral fibroblasts, oral human squamous carcinoma cells and macrophages in vitro. These data support the hypothesis that patients with cholestatic liver disease might benefit from UDCA with respect to periodontal health.