Objective The S100 calcium binding protein B (S100B) implicated in brain inflammation acts via the receptor of advanced glycation end products (RAGE) and is also secreted from adipocytes. We investigated the role of S100B in the interaction between adipocytes and macrophages using a cell-culture model. Design and Methods RAW264.7 macrophages (RAW) were stimulated by recombinant S100B to observe alterations in TNF-α and M1 markers; 3T3-L1 adipocytes (L1) were stimulated by TNF-α to examine S100B secretion. RAW and L1 were then mutually stimulated with conditioned media of each other, or co-cultured. The effects of S100B silencing or a RAGE-neutralizing antibody were also investigated. Results S100B upregulated TNF-α and M1 markers in RAW, and TNF-α augmented S100B secretion from L1. L1 conditioned media stimulated TNF-α secretion from RAW, and RAW conditioned media increased S100B secretion from L1. The co-culture of RAW and L1 increased TNF-α, S100B, and the expression of M1 markers and the MCP-1 receptor CCR2. The silencing of S100B or RAGE neutralization significantly ameliorated TNF-α hypersecretion from RAW that were stimulated with L1 conditioned media. Conclusions Thus, S100B as an adipokine may play a role in the interaction between adipocytes and macrophages to establish a vicious paracrine loop.
All Science Journal Classification (ASJC) codes
- Medicine (miscellaneous)
- Endocrinology, Diabetes and Metabolism
- Nutrition and Dietetics