Abstract
Adipocytes from white-adipose tissue are known to produce inflammatory cytokines, which play a major role in energy balance and metabolism. While they can respond to pathogen-associated molecular pattern (PAMPs) such as lipopolysaccharide (LPS) from bacteria, it is not known whether adipocytes can be stimulated by fungal cells. Previously, adipocytes were shown to produce toll-like receptor 2 (TLR2), a β-glucan receptor, suggesting that they could respond to β-glucan on the fungal cell wall. In this study, we show that heat-killed yeast induce an inflammatory response in adipocytes. Using fungal-like particles, namely laminarin-coated beads (LCB), we find that these particles trigger the expression of many key inflammatory genes in dose- and time-dependent fashions in adipocytes. These results suggest that β-glucan on the fungal cell wall is sufficient to elicit an inflammatory response in adipocytes. In addition, we show that both LCB and LCB-treated conditioned medium from RAW 264.7 murine macrophages (LCB-RM) induce the expression of those inflammatory genes through IKKβ-IκBα proteins. Together, we conclude that the fungal-like particles and the conditioned medium elicit an inflammatory response in adipocytes through the canonical or classical NF-κB pathway.
Highlights
Improper balance between excessive food intake and adipose tissue regulation results in obesity, which is a major epidemic problem worldwide
The expression levels of IL-6 and MCP-1/ CCL2 in differentiated 3T3-L1 adipocytes stimulated with LPS, zymosan, or an increasing amount of heat-killed Saccharomyces cerevisiae or Candida albicans were analyzed with quantitative PCR
We find that the expression of NF-κB1, IL-6, MCP-1/CCL2, and cyclooxygenase 2 (COX-2) genes are elevated as the increasing amount of laminarin-coated beads (LCB) or LCB-RM was added to the cells, suggesting a dose-dependent effect of both stimulators (Fig. 4A–D)
Summary
Improper balance between excessive food intake and adipose tissue regulation results in obesity, which is a major epidemic problem worldwide. The increase in circulating inflammatory cytokines during low-grade inflammation can be caused by several mechanisms, one of which involves the collaboration between adipocytes and immune cells in adipose tissue. The defect in the insulin signaling pathway in adipose tissue and skeletal muscles reduces their sensitivity to insulin, leading to the development of insulin resistance Consistent with this notion, mice with obesity induced by a high-fat diet develop insulin resistance[3]. The analysis of gene expression profile in adipose tissue isolated from mice with acute systemic inflammation induced by injection with LPS showed changes in the expression of over 6,000 genes, including the upregulation of TLR215 These studies suggest that adipocytes have the ability to recognize and respond to β-glucan on the fungal cell wall. It is possible that adipocytes may respond to β-glucan just like immune cells
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