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抗菌肽LL-37对牙龈卟啉单胞菌细胞及提取物诱导人牙龈成纤维细胞中IL-6、IL-8和CXCL10表达的抑制作用。

Suppressive effect of the antimicrobial peptide LL-37 on expression of IL-6, IL-8 and CXCL10 induced by Porphyromonas gingivalis cells and extracts in human gingival fibroblasts.

作者信息

Inomata Megumi, Into Takeshi, Murakami Yukitaka

机构信息

Department of Oral Microbiology, Asahi University, School of Dentistry, Mizuho, Gifu, Japan.

出版信息

Eur J Oral Sci. 2010 Dec;118(6):574-81. doi: 10.1111/j.1600-0722.2010.00775.x. Epub 2010 Sep 30.

Abstract

Porphyromonas gingivalis is a major periodontogenic bacterium and possesses immunostimulatory components, such as lipopolysaccharides (LPS) and fimbriae. The host antimicrobial peptide, LL-37, suppresses proinflammatory responses of immune cells but its effect on human gingival fibroblasts (HGFs) is not known. In this study, we assessed the effect of LL-37 on the proinflammatory responses of HGFs stimulated with P. gingivalis cells and their components. Live P. gingivalis cells did not induce proinflammatory responses of HGFs, and LL-37 did not alter these responses. However, LL-37 was able to suppress the killed P. gingivalis cell-induced secretion of interleukin (IL)-6 and IL-8. LL-37 also suppressed the expression of IL6, IL8, and CXCL10 genes that was induced by P. gingivalis components, including phenol-water extracts, lipid A, and fimbriae, and the induction of phosphorylation of p38 and extracellular signal-regulated kinase (ERK) by P. gingivalis lipopolysaccharide (LPS). CAMP was found to be expressed in oral epithelial cells but not in HGFs, despite stimulation with P. gingivalis components. Therefore, LL-37 can exert a suppressive effect on P. gingivalis-induced proinflammatory responses of HGFs in a paracrine manner, suggesting that excess inflammatory responses to P. gingivalis in the gingival tissue are suppressed by LL-37 in vivo.

摘要

牙龈卟啉单胞菌是一种主要的牙周致病菌,具有免疫刺激成分,如脂多糖(LPS)和菌毛。宿主抗菌肽LL-37可抑制免疫细胞的促炎反应,但其对人牙龈成纤维细胞(HGFs)的影响尚不清楚。在本研究中,我们评估了LL-37对牙龈卟啉单胞菌细胞及其成分刺激的HGFs促炎反应的影响。活的牙龈卟啉单胞菌细胞不会诱导HGFs的促炎反应,LL-37也不会改变这些反应。然而,LL-37能够抑制经热灭活的牙龈卟啉单胞菌细胞诱导的白细胞介素(IL)-6和IL-8的分泌。LL-37还抑制了牙龈卟啉单胞菌成分(包括酚水提取物、脂多糖A和菌毛)诱导的IL6、IL8和CXCL10基因的表达,以及牙龈卟啉单胞菌脂多糖(LPS)诱导的p38和细胞外信号调节激酶(ERK)的磷酸化。尽管受到牙龈卟啉单胞菌成分的刺激,但发现CAMP在口腔上皮细胞中表达,而在HGFs中不表达。因此,LL-37可以以旁分泌方式对牙龈卟啉单胞菌诱导的HGFs促炎反应发挥抑制作用,这表明体内LL-37抑制了牙龈组织中对牙龈卟啉单胞菌的过度炎症反应。

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