Trehalose inhibits inflammatory cytokine production by protecting IκB-α reduction in mouse peritoneal macrophages

Objective m of this study was to examine whether trehalose, a disaccharide, could inhibit Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS)-enhanced production of inflammatory cytokines in mouse peritoneal macrophages. peritoneal macrophages were treated with trehalose and stimulated with P. gingivalis LPS. Interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α) levels in the culture supernatant were measured by ELISA. The mRNA levels of the cytokines in macrophages were analysed by semi-quantitative RT-PCR. DNA and protein synthesis were measured by incorporation of [3H] thymidine or [14C] praline into mouse peritoneal macrophages. IκB-α reductions were assessed by western blot. s ent with trehalose suppressed LPS-induced IL-1β and TNF-α production and downregulated transcription of these cytokines. Furthermore, trehalose inhibited LPS-induced reduction of IκB-α. In addition, we also observed expression of the trehalose receptor (T1R3) in mouse peritoneal macrophages. sion results may suggest that trehalose inhibits LPS-induced production of IL-1β and TNF-α in mouse peritoneal macrophages by inhibiting degradation of IκB-α via the trehalose receptor T1R3.