HS mediates increased interleukin (IL)-1β and IL-18 production in leukocytes from patients with periodontitis.

: The mechanisms involved in the interplay between the bacteria and the host cells in periodontitis are not fully understood. : To investigate the effect of the bacterial metabolite HS 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 HS. : Subgingival bacterial samples from patients with periodontitis (N=32) and healthy controls (N=32) were investigated for HS production and bacterial composition. Peripheral blood mononuclear cells (PBMCs) were cultured in the presence/absence of 1mM HS for 24h and cytokine concentrations were measured. : Subgingival plaque from periodontitis patients had more HS producing bacteria and produced more HS, than healthy controls. PBMCs exposed to HS secreted significantly more IL-1ß and IL-18 (<0.0001) than untreated control PBMCs from both groups. PBMCs from the periodontitis patients secreted higher levels of the cytokines, both spontaneously (IL-1ß =0.0001; IL-18 =0.09) and after exposure to HS (IL-1ß =0.03; IL-18 =0.04), which is a new finding not previously reported. : HS, 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.