Stimulation of Toll-like receptors (TLR) induces an inflammatory reaction in many different cell types. TLRs signal via nuclear factor kB (NFkB). Activation of NFkB leads to its translocation from the cytoplasm into the nucleus where it induces transcription of inflammatory mediators, thus promoting inflammation. The severeness of an inflammation is controlled by the interaction of pro- and anti-inflammatory mediators. Recent evidence suggested the interaction between metabolism and immune defence. In this setting the hormones adiponectin and ghrelin have been reported to develop anti-inflammatory actions.

Therefore, their influence on two cell types involved in immune defence macrophages (murine RAW 264.7 cell line) and isolated human primary oral keratinocytes was investigated. Adiponectin and ghrelin as well as their receptors were detected by qRT-PCR in the macrophages and keratinocytes. TLR4 of both cell types was stimulated by lipopolysaccharide (LPS) and NFkB translocation was analyzed by immunofluorescence and western blot. In addition, pro- and anti-inflammatory cytokines were detected by qRT-PCR and ELISA after 4 and 24 h. In both cell types, adiponectin, ghrelin and their receptors were found to be expressed. LPS application enhanced the NFkB translocation leading to increased expression of inflammatory mediators (e.g. IL-1b, IL-6, IL-8, IL-10, MMP-1, -3). Incubation of the cells with full length adiponectin (1 mg/ml) and ghrelin (100 nM) significantly reduced the LPS-dependent NFkB translocation and expression of inflammatory mediators.

Both metabolic hormones exerted an anti-inflammatory influence via reduction of NFkB translocation independent of the cell type. This may contribute to the interaction between metabolism and immune reactions.