H(2)S mediates increased interleukin (IL)-1β and IL-18 production in leukocytes from patients with periodontitis

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 H(2)S 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 H(2)S. Methods: Subgingival bacterial samples from patients with periodontitis (N=32) and healthy controls (N=32) were investigated for H(2)S production and bacterial composition. Peripheral blood mononuclear cells (PBMCs) were cultured in the presence/absence of 1mM H(2)S for 24h and cytokine concentrations were measured. Results: Subgingival plaque from periodontitis patients had more H(2)S producing bacteria and produced more H(2)S, than healthy controls. PBMCs exposed to H(2)S 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 H(2)S (IL-1ß p=0.03; IL-18 p=0.04), which is a new finding not previously reported. Conclusions: H(2)S, 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.