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牙龈卟啉单胞菌的牙龈蛋白酶依赖性增强人牙龈上皮细胞中白细胞介素-33的产生。

Porphyromonas gingivalis Gingipain-Dependently Enhances IL-33 Production in Human Gingival Epithelial Cells.

作者信息

Tada Hiroyuki, Matsuyama Takashi, Nishioka Takashi, Hagiwara Makoto, Kiyoura Yusuke, Shimauchi Hidetoshi, Matsushita Kenji

机构信息

Department of Oral Disease Research, National Center for Geriatrics and Gerontology, Obu, Aichi, Japan.

Division of Oral Microbiology, Tohoku University Graduate School of Dentistry, Sendai, Miyagi, Japan.

出版信息

PLoS One. 2016 Apr 8;11(4):e0152794. doi: 10.1371/journal.pone.0152794. eCollection 2016.

Abstract

The cytokine IL-33 is constitutively expressed in epithelial cells and it augments Th2 cytokine-mediated inflammatory responses by regulating innate immune cells. We aimed to determine the role of the periodontal pathogen, Porphyromonas gingivalis, in the enhanced expression of IL-33 in human gingival epithelial cells. We detected IL-33 in inflamed gingival epithelium from patients with chronic periodontitis, and found that P. gingivalis increased IL-33 expression in the cytoplasm of human gingival epithelial cells in vitro. In contrast, lipopolysaccharide, lipopeptide, and fimbriae derived from P. gingivalis did not increase IL-33 expression. Specific inhibitors of P. gingivalis proteases (gingipains) suppressed IL-33 mRNA induction by P. gingivalis and the P. gingivalis gingipain-null mutant KDP136 did not induce IL-33 expression. A small interfering RNA for protease-activated receptor-2 (PAR-2) as well as inhibitors of phospholipase C, p38 and NF-κB inhibited the expression of IL-33 induced by P. gingivalis. These results indicate that the PAR-2/IL-33 axis is promoted by P. gingivalis infection in human gingival epithelial cells through a gingipain-dependent mechanism.

摘要

细胞因子白细胞介素-33(IL-33)在上皮细胞中持续表达,它通过调节天然免疫细胞增强Th2细胞因子介导的炎症反应。我们旨在确定牙周病原体牙龈卟啉单胞菌在人牙龈上皮细胞中IL-33表达增强中的作用。我们在慢性牙周炎患者的炎症牙龈上皮中检测到IL-33,并发现牙龈卟啉单胞菌在体外可增加人牙龈上皮细胞胞质中IL-33的表达。相比之下,牙龈卟啉单胞菌衍生的脂多糖、脂肽和菌毛不会增加IL-33的表达。牙龈卟啉单胞菌蛋白酶(牙龈蛋白酶)的特异性抑制剂可抑制牙龈卟啉单胞菌诱导的IL-33 mRNA表达,且牙龈卟啉单胞菌牙龈蛋白酶缺失突变体KDP136不会诱导IL-33表达。蛋白酶激活受体-2(PAR-2)的小干扰RNA以及磷脂酶C、p38和核因子κB的抑制剂可抑制牙龈卟啉单胞菌诱导的IL-33表达。这些结果表明,在人牙龈上皮细胞中,牙龈卟啉单胞菌感染通过一种依赖牙龈蛋白酶的机制促进PAR-2/IL-33轴的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a739/4825981/4b52a6b4b4c4/pone.0152794.g001.jpg

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