Lipoteichoic acid of Enterococcus faecalis interferes with Porphyromonas gingivalis lipopolysaccharide signaling via IRAK-M upregulation in human periodontal ligament cells.,Molecular Oral Microbiology

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Lipoteichoic acid of Enterococcus faecalis interferes with Porphyromonas gingivalis lipopolysaccharide signaling via IRAK-M upregulation in human periodontal ligament cells.
Molecular Oral Microbiology ( IF 2.8 ) Pub Date : 2020-05-29 , DOI: 10.1111/omi.12287
Jintaek Im ₁ , Jung Eun Baik ₁ , Dongwook Lee ₁ , Kee-Yeon Kum _{2,

3} , Cheol-Heui Yun ₄ , Ok-Jin Park ₁ , Seung Hyun Han ₁

Affiliation

Periodontitis is a chronic inflammatory disease of the gum caused by infection with multispecies oral bacteria. Since the periodontopathic bacteria, Porphyromonas gingivalis together with Enterococcus faecalis are frequently detected in patients with a severe form of periodontitis, interactions between their virulence factors might play an important role in progression of the disease. P. gingivalis and E. faecalis possess lipopolysaccharide (Pg.LPS) and lipoteichoic acid (Ef.LTA), respectively, as the major virulence factors inducing inflammatory responses. However, the combinatorial effect of these virulence factors on chemokine expression was poorly understood. Here, we examined the interaction between Ef.LTA and Pg.LPS on IL‐8 induction in human periodontal ligament (PDL) cells. Pg.LPS, but not Ef.LTA, induced IL‐8 expression at both mRNA and protein levels, which was suppressed in the presence of Ef.LTA. Although Ef.LTA and Pg.LPS could stimulate Toll‐like receptor 2 (TLR2), Ef.LTA did not interfere with Pg.LPS induced‐TLR2 activation. However, Ef.LTA decreased Pg.LPS‐induced phosphorylation of ERK, JNK, and p38 kinase. Furthermore, Ef.LTA suppressed Pg.LPS‐induced IL‐8 promoter activity as well as AP‐1, NF‐IL6 and NF‐κB transcription factors, which are indispensable for IL‐8 expression. Interestingly, Ef.LTA enhanced only IL‐1 receptor‐associated kinase‐M (IRAK‐M) expression among the tested negative regulators of TLR intracellular signaling cascades in the presence of Pg.LPS. In addition, silencing IRAK‐M restored the decreased IL‐8 expression by Ef.LTA in the presence of Pg.LPS. Collectively, these results suggest that Ef.LTA inhibits Pg.LPS‐induced IL‐8 expression in human PDL cells via inducing the expression of a negative regulator of TLR signaling cascades, IRAK‐M.

中文翻译：

粪肠球菌的脂磷壁酸通过IRAK-M上调在人牙周膜细胞中干扰牙龈卟啉单胞菌脂多糖信号传导。

牙周炎是由多种口腔细菌感染引起的牙龈的慢性炎性疾病。由于在患有严重形式的牙周炎的患者中经常检测到牙周病菌，牙龈卟啉单胞菌和粪肠球菌，它们的毒力因子之间的相互作用可能在疾病进展中起重要作用。牙龈卟啉单胞菌和粪肠球菌分别具有脂多糖（Pg.LPS）和脂磷壁酸（Ef.LTA）作为引起炎症反应的主要毒力因子。但是，这些毒力因子对趋化因子表达的组合作用了解甚少。在这里，我们检查了Ef.LTA和Pg.LPS之间在人牙周膜（PDL）细胞中IL-8诱导上的相互作用。Pg.LPS而不是Ef.LTA诱导了mRNA和蛋白质水平的IL-8表达，在Ef.LTA的存在下被抑制。尽管Ef.LTA和Pg.LPS可以刺激Toll样受体2（TLR2），但Ef.LTA不会干扰Pg.LPS诱导的TLR2激活。但是，Ef.LTA降低了Pg.LPS诱导的ERK，JNK和p38激酶的磷酸化。此外，Ef.LTA抑制了Pg.LPS诱导的IL-8启动子活性以及AP-1，NF-IL6和NF-κB转录因子，这对于IL-8表达是必不可少的。有趣的是，在存在Pg.LPS的情况下，经测试的TLR细胞内信号传导级联的负调节剂中，Ef.LTA仅增强IL-1受体相关的激酶M（IRAK-M）表达。此外，在存在Pg.LPS的情况下，沉默IRAK-M可恢复Ef.LTA降低的IL-8表达。总体而言，这些结果表明，Ef.LTA通过诱导TLR信号级联反应负调节剂IRAK-M的表达来抑制Pg.LPS诱导的人PDL细胞中IL-8的表达。在Pg.LPS存在下的LTA。总体而言，这些结果表明，Ef.LTA通过诱导TLR信号级联反应负调节剂IRAK-M的表达来抑制Pg.LPS诱导的人PDL细胞中IL-8的表达。在Pg.LPS存在下的LTA。总体而言，这些结果表明，Ef.LTA通过诱导TLR信号级联反应负调节剂IRAK-M的表达来抑制Pg.LPS诱导的人PDL细胞中IL-8的表达。

更新日期：2020-05-29

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