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Published on: May 4, 2021
TLR signalling and adapter utilization in primary human in vitro differentiated adipocytes
C Brenner1, R E Simmonds, S Wood
1Kennedy Institute of Rheumatology, Nuffield Department of Orthopaedics Rheumatology and Musculoskeletal Sciences, University of Oxford, London, UK.
Scandinavian Journal of Immunology
|June 14, 2012
Summary
Toll-like receptors (TLRs) in human adipocytes signal through distinct pathways. Lipopolysaccharide (LPS) and Pam3CSK4 use expected routes, while poly(I:C) signaling appears TRIF-independent but MyD88-dependent.
Area of Science:
- Immunology
- Cell Biology
- Metabolic Disease
Background:
- Toll-like receptors (TLRs) are crucial for innate immunity but are expressed beyond immune cells, including adipocytes.
- Adipocyte TLRs are implicated in obesity-associated pathologies like diabetes, yet their precise function remains unclear.
Purpose of the Study:
- To investigate Toll-like receptor (TLR) signaling pathways in primary human adipocytes.
- To identify the specific adapter molecules involved in TLR-mediated responses in these cells.
Main Methods:
- Primary human adipocytes were differentiated in vitro.
- Small interfering RNA (siRNA) was used to investigate the roles of adapter molecules like MyD88 and TRIF.
- Cells were stimulated with various TLR ligands, including lipopolysaccharide (LPS), poly(I:C), and Pam3CSK4.
- Cytokine production (IL-6, IL-8, MCP-1, IP-10) and IκBα degradation were assessed.
Main Results:
- LPS and Pam3CSK4 induced IL-6, IL-8, and MCP-1 production via TLR4 and TLR2, respectively, utilizing MyD88, Mal, and TRIF (for LPS) or MyD88 and Mal (for Pam3CSK4).
- Poly(I:C) strongly induced type I interferons (IP-10) and required MyD88 but not TRIF for NFκB-dependent cytokine induction.
- Poly(I:C) stimulation did not lead to rapid IκBα degradation, with IL-6 transcription observed at later time points (8-16 h).
Conclusions:
- Human adipocytes exhibit distinct TLR signaling routes.
- LPS and Pam3CSK4 signaling follows canonical pathways involving TLR4/TLR2 and specific adapter molecules.
- Poly(I:C) signaling via TLR3 in adipocytes appears to be TRIF-independent and MyD88-dependent, with delayed cytokine induction.
