Mendi Ayşegül, Köse Sevil, Uçkan Duygu, Akca Gülçin, Yilmaz Derviş, Aral Levent, Gültekin Sibel Elif, Eroğlu Tamer, Kiliç Emine, Uçkan Sina
Department of Medical Microbiology, Faculty of Dentistry, Gazi University, Ankara, Turkey.
PEDI-STEM Center for Stem Cell Research and Development, Hacettepe University, Ankara, Turkey.
J Appl Oral Sci. 2016 Jan-Feb;24(1):67-75. doi: 10.1590/1678-775720150145.
An increasing body of evidence suggests that the use of probiotic bacteria is a promising intervention approach for the treatment of inflammatory diseases with a polymicrobial etiology. P. gingivalis has been noted to have a different way of interacting with the innate immune response of the host compared to other pathogenic bacteria, which is a recognized feature that inhibits CXCL8 expression.
The aim of the study was to determine if P. gingivalis infection modulates the inflammatory response of gingival stromal stem cells (G-MSSCs), including the release of CXCL8, and the expression of TLRs and if immunomodulatory L. rhamnosus ATCC9595 could prevent CXCL8 inhibition in experimental inflammation.
G-MSSCs were pretreated with L. rhamnosus ATCC9595 and then stimulated with P. gingivalis ATCC33277. CXCL8 and IL-10 levels were investigated with ELISA and the TLR-4 and 2 were determined through flow cytometer analysis.
CXCL8 was suppressed by P. gingivalis and L. rhamnosus ATCC9595, whereas incubation with both strains did not abolish CXCL8. L. rhamnosus ATCC9595 scaled down the expression of TLR4 and induced TLR2 expression when exposed to P. gingivalis stimulation (p<0.01).
These findings provide evidence that L. rhamnosus ATCC9595 can modulate the inflammatory signals and could introduce P. gingivalis to immune systems by inducing CXCL8 secretion.
越来越多的证据表明,使用益生菌是治疗具有多种微生物病因的炎症性疾病的一种有前景的干预方法。与其他病原菌相比,牙龈卟啉单胞菌与宿主先天免疫反应的相互作用方式不同,这是一种公认的抑制CXCL8表达的特征。
本研究的目的是确定牙龈卟啉单胞菌感染是否会调节牙龈基质干细胞(G-MSSCs)的炎症反应,包括CXCL8的释放、Toll样受体(TLRs)的表达,以及免疫调节性鼠李糖乳杆菌ATCC9595是否能在实验性炎症中预防CXCL8的抑制。
用鼠李糖乳杆菌ATCC9595预处理G-MSSCs,然后用牙龈卟啉单胞菌ATCC33277刺激。用酶联免疫吸附测定法(ELISA)研究CXCL8和白细胞介素-10水平,通过流式细胞仪分析确定TLR-4和TLR-2。
牙龈卟啉单胞菌和鼠李糖乳杆菌ATCC9595均抑制CXCL8,但两种菌株共同孵育并未消除CXCL8。当暴露于牙龈卟啉单胞菌刺激时,鼠李糖乳杆菌ATCC9595下调TLR4的表达并诱导TLR2表达(p<0.01)。
这些发现提供了证据,表明鼠李糖乳杆菌ATCC9595可以调节炎症信号,并通过诱导CXCL8分泌将牙龈卟啉单胞菌引入免疫系统。