Possible roles of IL-33 in periodontal diseases: Porphyromonas gingivalis induced IL-33 in human gingival epithelial cells.
Possible roles of IL-33 in periodontal diseases: Porphyromonas gingivalis induced IL-33 in human gingival epithelial cells.
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IL-33 在牙周疾病中的可能作用：牙龈卟啉单胞菌在人牙龈上皮细胞中诱导 IL-33。
DOI：
10.1007/978-4-431-55192-8_25
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Kenji Matsushita
中科院分区：
文献类型：
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作者：
Hiroyuki Tada;Hidetoshi Shimauchi;Haruhiko Takada;Kenji Matsushita
在口腔粘膜中，上皮细胞不仅作为病原体的物理屏障，而且在启动对微生物的免疫反应中发挥关键作用。白细胞介素（IL）-33是IL-1家族的一员，在上皮细胞中组成性表达并增强Th 2型炎症免疫应答。我们发现IL-33在慢性牙周炎患者发炎的牙龈上皮中被检测到，牙周病牙龈卟啉单胞菌强烈增加人牙龈上皮细胞中IL-33 mRNA和分子的表达。相比之下，来自牙龈卟啉单胞菌的菌毛、脂肽和脂多糖在这方面没有活性。牙龈卟啉菌蛋白酶特异性的蛋白酶抑制剂有效地抑制由牙龈卟啉单胞菌刺激诱导的IL-33 mRNA。此外，牙龈卟啉单胞菌KDP 136，牙龈卟啉单胞菌蛋白酶无效突变体，没有增加IL-33 mRNA的表达。牙龈卟啉单胞菌通过蛋白酶活化受体2、磷脂酶C、丝裂原活化蛋白激酶p38和NF-κB上调IL-33 mRNA的表达。提示IL-33负性调节抗菌肽LL-37，导致慢性牙周炎牙龈上皮细胞天然免疫应答减弱。IL-33在口腔粘膜炎症中的可能作用进行了讨论。
In the oral mucosa, epithelial cells work not only as a physical barrier to pathogens, but also play a pivotal role in initiating immune responses to microbes. Interleukin (IL)-33, a member of the IL-1 family, is constitutively expressed in epithelial cells and amplifies Th2-type inflammatory immune responses. We found that IL-33 was detected in the inflamed gingival epithelium from chronic periodontitis patients, and periodontopathic Porphyromonas gingivalis strongly increased expressions of IL-33 mRNA and molecules in human gingival epithelial cells. In contrast, fimbriae, a lipopeptide and lipopolysaccharide derived from P. gingivalis were not active in this respect. Protease inhibitors specific for gingipains efficiently inhibited the induction of IL-33 mRNA by stimulation with P. gingivalis. Furthermore, P. gingivalis KDP136, a gingipains-null mutant, did not increase IL-33 mRNA expression. We also demonstrated that P. gingivalis upregulated IL-33 mRNA expression through protease-activated receptor-2, phospholipase C, mitogen-activated protein kinase p38 and NF-κB. IL-33 is suggested to negatively regulate antimicrobial peptide LL-37, resulting in attenuation of innate immune responses of gingival epithelial cells in chronic periodontitis. Possible roles of IL-33 in inflammation in the oral mucosa are discussed.