Colucci S, Mori G, Brunetti G, Coricciati M, Pignataro P, Oranger A, Cirulli N, Mastrangelo F, Grassi F R, Grano M
Department of Human Anatomy and Histology, University of Bari, Bari, Italy.
Int J Immunopathol Pharmacol. 2005 Jul-Sep;18(3 Suppl):13-9.
Periodontitis is characterized by irreversible destruction of alveolar bone and connective tissue attachment in the periodontium. We recently reported that T cells support the osteoclastogenesis by the overproduction of nuclear factor-kappa-B-ligand (RANKL) and Tumor Necrosis Factor-alpha (TNF-alpha) in an in vitro osteoclastogenesis model from periodontitis patients (Pp). It is known that IL-7 stimulates the production of osteoclastogenic factors by T cells and IL-6 potentiates IL-7 expression. Thus, we studied the involvement of IL-6 and IL-7 in the T cell regulation of osteoclast (OC) formation, in an in vitro osteoclastogenesis model from Pp. We demonstrated high levels of IL-7 in both the media collected from PBMC cultures of Pp and the sera of the same patients. We also demonstrated that freshly isolated B cells from PBMCs of Pp were the source of IL-7 in our model. B cells, in fact, overexpressed IL-7 at mRNA and protein levels, and this production was up-regulated by IL-6. Moreover, the OC formation decreased in the presence of anti-IL-6 and IL-7 functional antibodies in PBMC cultures from Pp. These data suggest that B cells could be responsible for the T cell-dependent osteoclastogenesis in periodontitis through the involvement of IL-6 and IL-7.
牙周炎的特征是牙周组织中牙槽骨和结缔组织附着的不可逆破坏。我们最近报道,在来自牙周炎患者(Pp)的体外破骨细胞生成模型中,T细胞通过过度产生核因子-κB配体(RANKL)和肿瘤坏死因子-α(TNF-α)来支持破骨细胞生成。已知白细胞介素-7(IL-7)刺激T细胞产生破骨细胞生成因子,白细胞介素-6(IL-6)增强IL-7的表达。因此,我们在来自Pp的体外破骨细胞生成模型中研究了IL-6和IL-7在T细胞对破骨细胞(OC)形成的调节中的作用。我们证明,从Pp的外周血单核细胞(PBMC)培养物收集的培养基和同一患者的血清中IL-7水平都很高。我们还证明,在我们的模型中,从Pp的PBMC中新鲜分离的B细胞是IL-7的来源。事实上,B细胞在mRNA和蛋白质水平上过表达IL-7,并且这种产生受到IL-6的上调。此外,在来自Pp的PBMC培养物中存在抗IL-6和IL-7功能性抗体时,OC形成减少。这些数据表明,B细胞可能通过IL-6和IL-7的参与,在牙周炎中导致T细胞依赖性破骨细胞生成。