Interleukin-13 Mediated Response in Periodontitis

Objectives: Periodontitis is an inflammatory disease of the supporting tissues of teeth. Interleukin (IL)-13 is a multifunctional Th2-originated cytokine which has a strong potential to diminish inflammatory responses. However the role of IL-13 in periodontitis is not fully understood yet. The purpose of this study was to investigate in vitro effects of IL-13 on the molecules involved in fibrosis and destruction, namely transforming growth factor-beta (TGF-β) and matrix metalloproteinases-1 (MMP-1).

Methods: Immunohistochemistry was used for localization of MMP-1 in periodontitis tissue samples. Enzyme-linked immunosorbent assays were performed to detect the levels of TGF-β and MMP-1, released from gingival fibroblast cell cultures following stimulation with IL-13 alone or in combination with tumor necrosis factor-α (TNF-α), respectively.

Results: Macrophage-like cells, fibroblast-like cells, vascular endothelial cells and gingival epithelial cells were more intensively stained for MMP-1 and also more frequent in periodontitis than in control group (P < 0.001). The cultured gingival fibroblasts with IL-13 produced TGF-β (P < 0.001) compared to non-stimulated cells. To mimic an inflammatory effect, TNF-α (10 ng/ML) was added and cell culture experiment was repeated on fibroblasts in combination with IL-13 (50 ng/mL). This further greatly diminished MMP-1 protein production, compared with that for TNF-α alone (P < 0.001).
Conclusions: The acquired data demonstrates that IL-13 has a role in the regulation of collagen homeostasis in gingival fibroblasts. IL-13 induces both upregulation of collagen (particularly TGF-β) and down-regulation of MMP-1 production. This effect may be strong in periodontitis and when Th2 cells provide T-cell help in intercellular cooperation.