Streptococcus mutans (S. mutans), a major aetiologic agent of dental caries, is involved in systemic diseases, such as bacterial endocarditis, if it enters the bloodstream through temporary bacteraemia. Interleukin (IL)-1β, a proinflammatory cytokine, is related to the host defences against pathogens, and its synthesis, maturation, and secretion are tightly regulated by the activation of the inflammasome, an inflammatory signalling complex. This study examined the signalling mechanism of IL-1β secretion and the inflammasome pathway induced by S. mutans to explain the molecular mechanism through which systemic infection by oral streptococci can occur. After infection of THP-1 cells with S. mutans, the expression of inflammasome components was detected using various methods. S. mutans induced IL-1β secretion via caspase-1 activation, and S. mutans-induced IL-1β secretion required absent in melanoma (AIM2), NLR family pyrin domain-containing 3 (NLRP3) and NLR family CARD domain-containing 4 (NLRC4) inflammasome activation. In particular, the S. mutans-induced NLRP3 inflammasome was mediated by adenosine triphosphate (ATP) release, potassium depletion and lysosomal damage. Our study provides novel insight into the innate immune response against S. mutans infection.

变形链球菌（S. mutans）是龋齿的主要病因，如果它通过暂时的菌血症进入血液，则会引起全身性疾病，例如细菌性心内膜炎。白细胞介素（IL）-1β是一种促炎细胞因子，与宿主对抗病原体的防御有关，其合成，成熟和分泌受到炎性体（炎性信号复合体）的激活的严格调控。这项研究检查了IL-1β分泌的信号传导机制和变形链球菌诱导的炎性体途径，以解释通过口腔链球菌发生全身感染的分子机制。变形链球菌感染THP-1细胞后，使用多种方法检测炎性体成分的表达。变形链球菌通过caspase-1激活诱导IL-1β分泌，而变形链球菌诱导的IL-1β分泌在黑色素瘤（AIM2），含NLR家族吡啶结构域3（NLRP3）和含NLR家族CARD结构域4中不存在（NLRC4）炎性体激活。特别地，变形链球菌诱导的NLRP3炎性体由三磷酸腺苷（ATP）释放，钾耗竭和溶酶体破坏介导。我们的研究提供了对变形链球菌感染的天然免疫反应的新见解。