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H2S mediates increased interleukin (IL)-1β and IL-18 production in leukocytes from patients with periodontitis

Artikel i vetenskaplig tidskrift
Författare Amina Basic
G. Serino
Åsa Leonhardt
Gunnar Dahlén
Publicerad i Journal of Oral Microbiology
Volym 11
Nummer/häfte 1
ISSN 2000-2297
Publiceringsår 2019
Publicerad vid Institutionen för odontologi
Institutionen för odontologi, sektion 3
Språk - English
Länkar doi.org/10.1080/20002297.2019.16170...
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Sammanfattning

- 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. © 2019, © 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

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