Background: The mechanisms involved in the interplay between the bacteria and the host cells in periodontitis are not fully understood.

Aim: To investigate the effect of the bacterial metabolite H₂S on the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 from periodontitis patients and healthy controls, and to evaluate the composition of the subgingival microbiota with its capacity to produce H₂S.

Methods: Subgingival bacterial samples from patients with periodontitis (N=32) and healthy controls (N=32) were investigated for H₂S production and bacterial composition. Peripheral blood mononuclear cells (PBMCs) were cultured in the presence/absence of 1mM H₂S for 24h and cytokine concentrations were measured.

Results: Subgingival plaque from periodontitis patients had more H₂S producing bacteria and produced more H₂S, than healthy controls. PBMCs exposed to H₂S secreted significantly more IL-1ß and IL-18 (p<0.0001) than untreated control PBMCs from both groups. PBMCs from the periodontitis patients secreted higher levels of the cytokines, both spontaneously (IL-1ß p=0.0001; IL-18 p=0.09) and after exposure to H₂S (IL-1ß p=0.03; IL-18 p=0.04), which is a new finding not previously reported.

Conclusions: H₂S, from the subgingival microbiota, can contribute to a host inflammatory response through secretion of the pro-inflammatory cytokines IL-1β and IL-18. Since this response differs between individuals, it may also reflect the susceptibility of the host to develop periodontitis.

背景：牙周炎中细菌与宿主细胞之间相互作用的机制尚不完全清楚。

目的：研究细菌代谢产物H ₂ S对牙周炎患者和健康对照者促炎性细胞因子白介素（IL）-1β和IL-18的影响，并评估龈下微生物群的组成及其产生能力ħ ₂ S.

方法：调查牙周炎患者（N = 32）和健康对照者（N = 32）的龈下细菌样品中H ₂ S的产生和细菌组成。在存在/不存在1mM H ₂ S的情况下，将外周血单个核细胞（PBMC）培养24小时，并测量细胞因子浓度。

结果：从牙周炎患者龈下菌斑有多个H ₂小号产生菌和生产多个H ₂ S，高于健康对照。暴露至H的PBMC ₂ š显著分泌更多的IL-1β和IL-18（p大于从两组未处理的对照的PBMC <0.0001）。从牙周炎患者的PBMC分泌的更高水平的细胞因子，包括自发（IL-1β p = 0.0001; IL-18 p = 0.09）和曝光后至H ₂ S（IL-1β p = 0.03; IL-18 p = 0.04 ），这是以前未报告的新发现。

结论：龈下菌群中的H ₂ S可通过促炎细胞因子IL-1β和IL-18的分泌来促进宿主的炎症反应。由于个体之间的反应不同，因此也可能反映出宿主发展成牙周炎的敏感性。