Department of Microbiology, Nippon Dental University School of Life Dentistry at Tokyo, Tokyo, Japan.
Odontology. 2012 Jul;100(2):144-8. doi: 10.1007/s10266-011-0044-z. Epub 2011 Oct 18.
Infective endocarditis is frequently attributed to oral streptococci. Although the pathogenetic mechanisms are not well understood, interaction between streptococci and phagocytes is thought to be important for infective endocarditis. In this study, HL-60 cell-derived monocytes were characterized following interaction with Streptococcus gordonii DL1. Exposure of monocytes to S. gordonii DL1 induced up-regulation of the dendritic cell (DC) markers CD83, CD1a, CD86, and interleukin-12, while monocyte markers PU.1 and MafB, which are typically present at low levels in mature DCs, were down-regulated. Interaction of HL-60-derived monocytes with S. gordonii DL1 was instructive for DC differentiation in the absence of released cytokines. Furthermore, neither the filtered culture medium of S. gordonii nor the hsa mutant, deficient in sialic acid-binding activity, was able to induce the differentiation of HL-60 cells. Taken together, these data suggest that monocytes stimulated with S. gordonii DL1 rapidly undergo monocyte-to-DC differentiation through interaction with the bacterial surface receptor Hsa and that this response may be the initial step in infective endocarditis by oral streptococci.
感染性心内膜炎常归因于口腔链球菌。尽管发病机制尚不清楚，但链球菌与吞噬细胞的相互作用被认为对感染性心内膜炎很重要。在这项研究中，HL-60 细胞衍生的单核细胞与戈登链球菌 DL1 相互作用后进行了特征描述。单核细胞暴露于 S. gordonii DL1 会诱导树突状细胞 (DC) 标志物 CD83、CD1a、CD86 和白细胞介素-12 的上调，而通常在成熟 DC 中低水平表达的单核细胞标志物 PU.1 和 MafB 则下调。HL-60 衍生的单核细胞与 S. gordonii DL1 的相互作用在没有释放细胞因子的情况下对 DC 分化具有指导作用。此外，戈登链球菌的过滤培养液或缺乏唾液酸结合活性的 hsa 突变体均不能诱导 HL-60 细胞分化。综上所述，这些数据表明，用 S. gordonii DL1 刺激的单核细胞通过与细菌表面受体 Hsa 的相互作用迅速经历单核细胞向 DC 的分化，并且该反应可能是口腔链球菌引起感染性心内膜炎的初始步骤。
