Increased Toll-like receptor (TLR) mRNA expression in monocytes is a feature of metabolic syndrome in adolescents
Article first published online: 19 SEP 2012
© 2012 The Authors. Pediatric Obesity © 2012 International Association for the Study of Obesity
Volume 8, Issue 1, pages e19–e23, February 2013
How to Cite
Hardy, O. T., Kim, A., Ciccarelli, C., Hayman, L. L. and Wiecha, J. (2013), Increased Toll-like receptor (TLR) mRNA expression in monocytes is a feature of metabolic syndrome in adolescents. Pediatric Obesity, 8: e19–e23. doi: 10.1111/j.2047-6310.2012.00098.x
- Issue published online: 7 JAN 2013
- Article first published online: 19 SEP 2012
- Manuscript Accepted: 1 AUG 2012
- Manuscript Revised: 24 JUL 2012
- Manuscript Received: 25 JUN 2012
- UMass Center for Clinical and Translational Science. Grant Number: UL1RR031982
- Life Sciences Moment Fund
- Diabetes Endocrinology Research Center. Grant Number: DK32520
- innate immunity;
- metabolic syndrome;
Metabolic syndrome (MetSyn) is diagnosed frequently in some but not all overweight adolescents. Chronic inflammation, as seen in obesity, is strongly associated with MetSyn.
The aim of this pilot study was to assess the correlation between activation of the innate immune system and MetSyn, independent of body mass index (BMI), in a young population.
We quantitatively measured both systemic pro-inflammatory cytokines and gene expression of Toll-like receptors (TLRs) and downstream cytokines in circulating monocytes obtained from nine adolescents with metabolic syndrome (Overwt-MetSyn) and eight BMI-matched controls (Overwt-Healthy).
The Overwt-MetSyn group demonstrated a significant elevation in expression of TLR2, TLR4, tumour necrosis factor-a (TNF a) and interleukin-6 (IL6) in peripheral monocytes, and increased circulating levels of TNF a and IL6 when compared with the Overwt-Healthy group. TLR2 (r = 0.78, P < 0.001), TLR4 (r = 0.57, P < 0.01) and TNF a (r = 0.61, P < 0.01) gene expression positively correlated with serum levels of TNF a.
Our study suggests that activation of the innate immune pathway via TLRs may be partially responsible for the increased systemic inflammation seen in adolescents with MetSyn.