Liu Jiarong, Chen Jie, Du Xingyan, Hu Li, Chen Lili
Department of Stomatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, PR China.
Arch Oral Biol. 2014 Feb;59(2):193-8. doi: 10.1016/j.archoralbio.2013.11.007. Epub 2013 Nov 23.
Although the secretion of antimicrobial peptides in gingival tissue and isolated cells has been reported, the induction of human β-defensins (hBDs) in epithelial cells from the periodontitis patients was not stated before. This study aimed to compare the secretion of hBDs in gingival epithelial cells from periodontitis patients and healthy controls.
Firstly, gingival biopsies were obtained from chronic periodontitis patients and healthy controls and the hBDs expression level in gingival tissues was quantified. Then the epithelial cells from periodontitis patients and healthy controls were isolated and challenged with different concentrations of tumour necrosis factor-alpha (TNFα). The hBDs expression level was also quantified after induction. At last, to identify the molecular pathways involved in hBDs induction, the isolated cells were incubated with NF-kB or MAPK inhibitor before TNFα induction.
Higher hBDs expression was found in gingival tissues from healthy controls. The in vitro experiments demonstrated that the hBD-2 expression in gingival epithelial cells from periodontitis patients can be induced by TNFα at lower dose, while the optimum expression level was much lower. The basal hBD-3 mRNA expression was much higher in cells from periodontitis patients. The molecular pathways involved in the responses to the inflammatory cytokine in patients and healthy controls were the same.
The epithelial cells from periodontitis patients are more prone to recognize and respond to TNFα to produce hBD-2. The basal expression of hBD-3 in keratinocytes from periodontitis patients suggested that hBD-3 may play an important role in the immunological reaction against periodontitis.
尽管已有报道称牙龈组织和分离细胞中存在抗菌肽分泌，但此前未提及牙周炎患者上皮细胞中人β-防御素（hBDs）的诱导情况。本研究旨在比较牙周炎患者和健康对照者牙龈上皮细胞中hBDs的分泌情况。
首先，从慢性牙周炎患者和健康对照者获取牙龈活检组织，对牙龈组织中hBDs的表达水平进行定量。然后分离牙周炎患者和健康对照者的上皮细胞，并用不同浓度的肿瘤坏死因子-α（TNFα）进行刺激。诱导后也对hBDs的表达水平进行定量。最后，为确定参与hBDs诱导的分子途径，在TNFα诱导前将分离的细胞与NF-κB或MAPK抑制剂孵育。
在健康对照者的牙龈组织中发现更高的hBDs表达。体外实验表明，较低剂量的TNFα可诱导牙周炎患者牙龈上皮细胞中hBD-2的表达，但其最佳表达水平要低得多。牙周炎患者细胞中hBD-3的基础mRNA表达要高得多。患者和健康对照者对炎性细胞因子反应所涉及的分子途径相同。
牙周炎患者的上皮细胞更易于识别并对TNFα作出反应以产生hBD-2。牙周炎患者角质形成细胞中hBD-3的基础表达表明，hBD-3可能在针对牙周炎的免疫反应中起重要作用。
