Lipoxin suppresses inflammation via the TLR4/MyD88/NF-κB pathway in periodontal ligament cells

Objective The objective of the present study was to evaluate the anti-inflammatory effects of lipoxin A4 (LXA4) for the treatment of periodontitis in an in vitro model. Methods Human PDLCs were challenged with Escherichia coli (E. coli) lipopolysaccharide (LPS) to evoke an inflammatory response. This was done either in monoculture or in coculture with THP-1, a monocytic cell line. Thereafter, cytokine expression was measured by ELISA, with or without LXA4. In addition, the effects of LXA4 were analyzed on the TLR-MyD88-NF-kappa B (TMN)-mediated intracellular signal pathway using immunocytochemistry. Results In response to LPS, the level of the pro-inflammatory cytokine tumor necrosis factor alpha increased, whereas the anti-inflammatory cytokine interleukin-4 decreased significantly (p < .05). These effects were consistently reversed when LPS-challenged PDLCs were also treated with LXA4. The results in the coculture system were comparable to the monoculture. Immunohistochemistry and quantitative assessment confirmed the importance of the TMN signal pathway in these processes. Conclusion These results corroborate earlier findings that PDLCs play an important role in inflammation. Moreover, LXA4 might offer new approaches for the therapeutic treatment of periodontal disease.