Streptococcus mutans is a causative organism of dental caries and has been reported to be associated with the development of cardiovascular disease (CVD). Previous studies have demonstrated that S. mutans invades human aortic endothelial cells (HAECs) and HAECs invaded by S. mutans produce higher levels of CVD–related cytokines than non‐invaded HAECs. DMBT1 (deleted in malignant brain tumors 1), also known as salivary agglutinin or gp‐340, belongs to the scavenger receptor cysteine–rich superfamily. DMBT1 is expressed in epithelial and non‐epithelial tissues and has multiple functions. The interaction between S. mutans and DMBT1 has been demonstrated in cariogenesis, but DMBT1 involvement in CVD has not been examined. In this study, we investigated DMBT1 expression in HAECs stimulated with S. mutans and examined the role of DMBT1 in the interaction between S. mutans and HAECs. All of the tested S. mutans strains induced higher production levels of DMBT1 in HAECs than those in unstimulated HAECs. More S. mutans cells adhered to DMBT1 knock down HAECs than to DMBT1–producing HAECs. Invasion of DMBT1 knock down HAECs by S. mutans was stronger than that of DMBT1–producing HAECs, and externally added DMBT1 reduced bacterial invasion. Cytokine production by DMBT1 knock down HAECs by S. mutans stimulation was higher than that by DMBT1–producing HAECs. These phenomena seemed to be due to the effect of released DMBT1, namely, the inhibition of bacterial adherence to HAECs by DMBT1. These results suggest that DMBT1 plays a protective role against the S. mutans–induced CVD process in HAECs.

中文翻译：

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DMBT1参与人主动脉内皮细胞对变形链球菌的反应。

变形链球菌是龋齿的致病生物，据报道与心血管疾病（CVD）的发展有关。先前的研究表明，变形链球菌入侵人主动脉内皮细胞（HAEC），而变形链球菌入侵的HAEC产生的CVD相关细胞因子水平高于未入侵的HAEC。DMBT1（在恶性脑瘤1中已删除），也称为唾液凝集素或gp-340，属于富含清道夫受体的半胱氨酸超家族。DMBT1在上皮和非上皮组织中表达，并具有多种功能。变形链球菌之间的相互作用DMBT1已在龋发生中得到证实，但尚未检查DMBT1是否参与CVD。在这项研究中，我们调查了变形链球菌刺激的HAEC中DMBT1的表达，并探讨了DMBT1在变形链球菌与HAEC之间相互作用中的作用。与未经刺激的HAEC相比，所有测试的变形链球菌菌株在HAEC中诱导的DMBT1产量更高。与产生DMBT1的HAEC相比，粘附于DMBT1的HA.s变异链球菌细胞更多。变形链球菌对DMBT1的敲低HAEC的入侵要强于产生DMBT1的HAEC，而外部添加的DMBT1则减少了细菌的入侵。DMBT1产生的细胞因子可降低变形链球菌的HAEC刺激高于产生DMBT1的HAEC。这些现象似乎是由于释放的DMBT1的作用所致，即DMBT1抑制细菌对HAEC的粘附。这些结果表明，DMBT1对变形链球菌诱导的HAEC中的CVD过程起保护作用。