Al-Samadi A, Salem A, Ainola M, Hietanen J, Häyrinen-Immonen R, Konttinen Y T
Department of Medicine, Institute of Clinical Medicine, University of Helsinki, Helsinki, Finland; Department of Anatomy, Institute of Biomedicine, University of Helsinki, Helsinki, Finland.
Oral Dis. 2015 Apr;21(3):292-8. doi: 10.1111/odi.12262. Epub 2014 Jun 25.
It was hypothesized that beta 2 defensin (BD-2) is increased in RAU lesions compared with healthy controls to promote anti-microbial host defence.
RAU and control mucosa samples were subjected to quantitative real-time PCR and immunostained for BD-2, CD68, mast cell tryptase and 4-hydroxynonenal (4HNE). The effect of tumour necrosis factor-α (TNF-α) ± interleukin-17C (IL-17C), without and with vitamin K3, was studied on BD-2 expression in epithelial SCC-25 cells.
Although BD-2 mRNA did not differ between healthy and RAU mucosa, BD-2 stained strongly in acute-phase RAU epithelium (P = 0.001). In controls, subepithelial BD-2(+) cells were mast cells and macrophages, whereas in RAU, most infiltrating leucocytes were BD-2(+) (P = 0.004). In cell culture, BD-2 was increased 124-fold by TNF-α (P < 0.0001) and 208-fold synergistically together with IL-17C (P < 0.0001). 4HNE staining of RAU epithelium was not significantly increased, and vitamin K3-induced reactive oxygen species (ROS) did not affect BD-2.
Anti-microbial BD-2 was not affected by oxidative stress but was highly increased in the epithelial and immigrant cells in the acute-phase RAU lesions, probably in part synergistically by TNF-α and epithelial IL-17C, which are known to be induced by activation of danger-signal receptors by pathogen- and/or damage-associated molecular patterns.
据推测，与健康对照相比，复发性阿弗他溃疡（RAU）病变中β2防御素（BD-2）增加，以促进宿主的抗微生物防御。
对RAU和对照黏膜样本进行定量实时PCR，并对BD-2、CD68、肥大细胞类胰蛋白酶和4-羟基壬烯醛（4HNE）进行免疫染色。研究了肿瘤坏死因子-α（TNF-α）±白细胞介素-17C（IL-17C）在有无维生素K3情况下对上皮性SCC-25细胞中BD-2表达的影响。
尽管健康黏膜和RAU黏膜之间BD-2 mRNA没有差异，但BD-2在急性期RAU上皮中染色强烈（P = 0.001）。在对照中，上皮下BD-2(+)细胞是肥大细胞和巨噬细胞，而在RAU中，大多数浸润白细胞是BD-2(+)（P = 0.004）。在细胞培养中，TNF-α使BD-2增加124倍（P < 0.0001），与IL-17C协同作用使其增加208倍（P < 0.0001）。RAU上皮的4HNE染色没有显著增加，维生素K3诱导的活性氧（ROS）不影响BD-2。
抗微生物BD-2不受氧化应激影响，但在急性期RAU病变的上皮细胞和浸润细胞中高度增加，可能部分是由TNF-α和上皮IL-17C协同作用所致，已知它们是由病原体和/或损伤相关分子模式激活危险信号受体所诱导。
