Abstract
BackgroundB cell activating factor (BAFF) is a member of the tumor necrosis factor (TNF) superfamily with immunomodulatory effects on both innate and adaptive immune responses. Periodontitis is an inflammatory disease characterized by periodontal soft tissue inflammation and the progressive loss of periodontal ligament and alveolar bone. Macrophages are closely related to periodontitis progression. However, the role of BAFF in periodontitis development and macrophage polarization and the underlying mechanism remain unknown.MethodsIn vivo, a ligation-induced mouse model of periodontitis for BAFF blockade was established to investigate the expression of inducible nitric oxide synthase (iNOS) through real-time PCR (RT-PCR) and immunohistochemistry. In addition, the level of TNF-α in the periodontium, the number of osteoclasts, and alveolar bone resorption were observed. In vitro, RAW 264.7 macrophage cells were treated with 100 ng/mL Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS) in either the presence or absence of 50 nM small interfering RNA (siRNA) targeting BAFF, followed by further incubation for 24 h. These cells and supernatants were collected and stored for RT-PCR, enzyme-linked immunosorbent assay, western blotting and immunofluorescence microscopy.ResultsIn vivo, BAFF blockade decreased the levels of TNF-α in the periodontium in a ligature-induced mouse periodontitis model. Reduced osteoclast formation and lower alveolar bone loss were also observed. In addition, BAFF blockade was related to the expression of polarization signature molecules in macrophages. In vitro, BAFF knockdown notably suppressed the production of TNF-α in RAW 264.7 cells stimulated by P. gingivalis LPS. Moreover, BAFF knockdown attenuated the polarization of RAW 264.7 cells into classically activated macrophages (M1), with reduced expression of iNOS.ConclusionsBased on our limited evidence, we showed BAFF blockade exhibits potent anti-inflammatory properties in mice experimental periodontitis in vivo and in P. gingivalis LPS-treated RAW 264.7 cells in vitro, and macrophage polarization may be responsible for this effect.
Highlights
B cell activating factor (BAFF) is a member of the tumor necrosis factor (TNF) superfamily with immu‐ nomodulatory effects on both innate and adaptive immune responses
Expression of BAFF in a periodontitis mouse model To evaluate the involvement of BAFF in the periodontitis model, we first developed a periodontitis mouse model as described in the Methods section (Fig. 2a), and the expression of BAFF was determined on day 14 after the induction
We found that the tumor necrosis factor-α (TNF-α) mRNA expression was significantly increased in the periodontitis group compared to that in the control group. (Fig. 2d)
Summary
B cell activating factor (BAFF) is a member of the tumor necrosis factor (TNF) superfamily with immu‐ nomodulatory effects on both innate and adaptive immune responses. Periodontitis is an inflammatory disease char‐ acterized by periodontal soft tissue inflammation and the progressive loss of periodontal ligament and alveolar bone. Periodontitis is an inflammatory disease characterized by periodontal soft tissue inflammation and progressive loss of the periodontal ligament and alveolar bone, which may eventually cause tooth loss [1, 2]. Macrophages are an important part of host immunity as they recognize, phagocytize, and remove foreign pathogens and foreign bodies. They can secrete a variety of cytokines to regulate the immune response and activate adaptive immunity, playing an important role in the immune system. Many studies have shown that macrophages are closely related to the progression of periodontitis [8, 9]
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