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Leptin up-regulates TLR2 in human monocytes.
Katrin M Jaedicke1, Ashleigh Roythorne, Kay Padget
1Newcastle University, Framlington Place, Newcastle upon Tyne, UK. katrin.jaedicke@ncl.ac.uk
Journal of Leukocyte Biology
|January 24, 2013
Summary
Leptin, elevated in obesity and T2DM, increases Toll-like receptor 2 (TLR2) expression on monocytes. This suggests leptin may enhance innate immunity and inflammation in metabolic diseases.
Area of Science:
- Immunology
- Endocrinology
- Molecular Biology
Background:
- Leptin, an adipokine, influences immune cell activation markers.
- Elevated serum leptin is linked to obesity and type 2 diabetes mellitus (T2DM), conditions associated with inflammation.
- The effect of leptin on pattern recognition receptors (PRRs) in monocytes is not well understood.
Purpose of the Study:
- To investigate the role of leptin in regulating Toll-like receptor (TLR) and CD14 expression in monocytes.
- To determine if leptin influences monocyte responses to lipopolysaccharide (LPS).
Main Methods:
- THP-1 cells and primary human monocytes were stimulated with leptin.
- Cell-surface and mRNA expression of TLR2, TLR4, and CD14 were analyzed.
- Expression of transcription factors PU.1 and EGR2 was assessed.
- Leptin's effect on LPS-induced TNF-α secretion was measured.
Main Results:
- Leptin increased both cell-surface and mRNA expression of TLR2 in monocytes.
- Leptin did not affect TLR4 expression.
- CD14 expression increased in THP-1 cells but not primary monocytes.
- Leptin up-regulated transcription factors PU.1 and EGR2.
- Leptin enhanced LPS-induced TNF-α secretion.
Conclusions:
- Leptin differentially influences monocyte phenotype compared to LPS.
- Leptin up-regulates monocyte TLR2 expression, a novel finding.
- Leptin-stimulated TLR2 may enhance innate immunity and inflammation in hyperleptinemic states like obesity and T2DM.
