Porphyromonas gingivalis induces the production of interleukin-31 by human mast cells, resulting in dysfunction of the gingival epithelial barrier.
Porphyromonas gingivalis induces the production of interleukin-31 by human mast cells, resulting in dysfunction of the gingival epithelial barrier.
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牙龈卟啉单胞菌诱导人类肥大细胞产生白细胞介素 31，导致牙龈上皮屏障功能障碍。
DOI：
10.1111/cmi.12972
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Matsushita Kenji.
中科院分区：
文献类型：
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作者：
Tada Hiroyuki;Nishioka Takashi;Takase Aya;Numazaki Kento;Bando Kanan;Matsushita Kenji.
白细胞介素（IL）-31对粘膜组织和皮肤的先天免疫很重要，IL-31表达增加参与影响皮肤、气道、肺和肠的慢性炎性疾病的发病机制。我们研究了肥大细胞在牙周病原体牙龈卟啉单胞菌感染后诱导IL-31产生的作用。我们发现口腔感染牙龈卟啉单胞菌增加了野生型小鼠牙龈组织中IL-31的表达，但在肥大细胞缺陷型小鼠中则没有。牙龈卟啉单胞菌诱导的人肥大细胞产生IL-31是通过激活JNK和NF-κB信号通路发生的，并且依赖于牙龈卟啉单胞菌赖氨酸特异性蛋白酶牙龈卟啉单胞菌蛋白酶-牙龈卟啉单胞菌感染诱导的人牙龈上皮细胞中IL-31受体α和抑瘤素M受体β的表达。值得注意的是，牙龈卟啉单胞菌诱导肥大细胞产生IL-31，导致牙龈上皮细胞中紧密连接分子claudin-1的下调，导致牙龈上皮屏障的细胞旁渗透性的IL-31依赖性增加。这些结果表明，肥大细胞对牙龈卟啉单胞菌感染产生的IL-31导致牙龈上皮屏障功能障碍，这可能有助于牙周炎中观察到的慢性炎症。
Interleukin (IL)‐31 is important for innate immunity in mucosal tissues and skin, and increased IL‐31 expression participates in the pathogenesis of chronic inflammatory diseases affecting the skin, airways, lungs, and intestines. We investigated the contribution of mast cells to the induction of IL‐31 production following infection with the periodontal pathogen,Porphyromonas gingivalis. We found that oral infection withP. gingivalisincreased IL‐31 expression in the gingival tissues of wild‐type mice but not in those of mast cell‐deficient mice. TheP. gingivalis‐induced IL‐31 production by human mast cells occurred through the activation of the JNK and NF‐κB signalling pathways and was dependent on theP. gingivalislysine‐specific protease gingipain‐K.P. gingivalisinfection induced IL‐31 receptor α and oncostatin M receptor β expression in human gingival epithelial cells. Notably, theP. gingivalis‐induced IL‐31 production by mast cells led to the downregulation of claudin‐1, a tight junction molecule, in gingival epithelial cells, resulting in an IL‐31‐dependent increase in the paracellular permeability of the gingival epithelial barrier. These findings suggest that IL‐31 produced by mast cells in response toP. gingivalisinfection causes gingival epithelial barrier dysfunction, which may contribute to the chronic inflammation observed in periodontitis.