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Published on: July 17, 2018
Fungal-like particles and macrophage-conditioned medium are inflammatory elicitors for 3T3-L1 adipocytes
Chanawee Jakkawanpitak1, Nongporn Hutadilok-Towatana1, Decha Sermwittayawong2
1Department of Biochemistry, Faculty of Science, Prince of Songkla University, Hat Yai, 90110, Thailand.
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.
Insights
White fat cells can be activated by fungal components, triggering an inflammatory response. This suggests a new pathway for immune signaling in metabolic tissues.
Area of Science:
- Immunology
- Metabolism
- Cell Biology
Background:
- Adipocytes produce inflammatory cytokines crucial for energy balance and metabolism.
- White adipocytes respond to bacterial pathogen-associated molecular patterns (PAMPs) like lipopolysaccharide (LPS).
- Adipocytes express toll-like receptor 2 (TLR2), a receptor for fungal β-glucans, hinting at fungal recognition capabilities.
Purpose of the Study:
- To investigate whether adipocytes can be stimulated by fungal cells or their components.
- To determine if fungal β-glucans are sufficient to elicit an inflammatory response in adipocytes.
- To elucidate the signaling pathway involved in adipocyte inflammatory response to fungal stimuli.
Main Methods:
- Stimulation of adipocytes with heat-killed yeast and fungal-like particles (laminarin-coated beads, LCB).
- Analysis of inflammatory gene expression in adipocytes.
- Investigation of the involvement of IKKβ-IκBα proteins and the NF-κB pathway.
Main Results:
- Heat-killed yeast and LCB induced an inflammatory response in adipocytes.
- LCB triggered the dose- and time-dependent expression of key inflammatory genes.
- Both LCB and LCB-conditioned macrophage medium activated inflammatory gene expression via the IKKβ-IκBα pathway.
Conclusions:
- Fungal β-glucans are sufficient to elicit an inflammatory response in adipocytes.
- Adipocytes respond to fungal components through the canonical NF-κB signaling pathway.
- This study reveals a novel mechanism of immune recognition and inflammatory signaling in white adipose tissue.
