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Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
Published on: April 3, 2017
Systemic inflammation in childhood obesity: circulating inflammatory mediators and activated CD14++ monocytes
H S Schipper1,2, R Nuboer3, S Prop1
1Department of Metabolic Diseases, University Medical Center Utrecht, Room STR3.217, Universiteitsweg 100, 3584 CG, Utrecht, the Netherlands.
Insights
Childhood obesity activates inflammatory pathways, including increased inflammatory mediators and CD14(++) monocyte activation, linking it to metabolic and cardiovascular risks early in life.
Area of Science:
- Pediatric Endocrinology
- Immunology
- Cardiovascular Health
Background:
- Obesity in adults is linked to inflammation and cardiovascular issues via mediators and CD14(++) monocytes.
- It remains unclear if these inflammatory changes manifest in childhood obesity.
- This study investigates early inflammatory alterations in pediatric obesity.
Purpose of the Study:
- To comprehensively analyze circulating inflammatory mediators in childhood obesity.
- To assess monocyte populations and their functional status in obese children.
- To identify early inflammatory markers associated with obesity-related complications.
Main Methods:
- Measured 35 circulating inflammatory mediators, including adipokines, in lean and obese children (6-16 years).
- Utilized hierarchical cluster analysis to associate inflammatory profiles with clinical variables.
- Performed monocyte phenotyping and functional assays using lipopolysaccharide stimulation.
Main Results:
- Identified chemerin, tissue inhibitor of metalloproteinase 1, EGF, and TNF receptor 2 as novel inflammatory mediators elevated in childhood obesity.
- Cluster analysis revealed distinct inflammatory profiles and clinical differences across obesity and leanness clusters.
- Childhood obesity correlated with higher CD14(++) monocyte counts and an activated monocyte phenotype.
Conclusions:
- Inflammatory mediator profiles cluster and associate with insulin resistance in both obese and lean children.
- Activated CD14(++) monocyte subsets, linked to atherosclerosis, are present in obese children.
- Inflammatory mechanisms contributing to obesity complications are active from childhood.
Aims/Hypothesis:
In adults, circulating inflammatory mediators and activated CD14(++) monocytes link obesity to its metabolic and cardiovascular complications. However, it is largely unknown whether these inflammatory changes already occur in childhood obesity. To survey inflammatory changes during the early stages of obesity, we performed a comprehensive analysis of circulating inflammatory mediators, monocyte populations and their function in childhood obesity.
Methods:
In lean and obese children aged 6 to 16 years (n = 96), 35 circulating inflammatory mediators including adipokines were measured. Hierarchical cluster analysis of the inflammatory mediator profiles was performed to investigate associations between inflammatory mediator clusters and clinical variables. Whole-blood monocyte phenotyping and functional testing with the toll-like receptor 4 ligand, lipopolysaccharide, were also executed.
Results:
First, next to leptin, the circulating mediators chemerin, tissue inhibitor of metalloproteinase 1, EGF and TNF receptor 2 were identified as novel inflammatory mediators that are increased in childhood obesity. Second, cluster analysis of the circulating mediators distinguished two obesity clusters, two leanness clusters and one mixed cluster. All clusters showed distinct inflammatory mediator profiles, together with differences in insulin sensitivity and other clinical variables. Third, childhood obesity was associated with increased CD14(++) monocyte numbers and an activated phenotype of the CD14(++) monocyte subsets.
Conclusions/Interpretation:
Inflammatory mediator clusters were associated with insulin resistance in obese and lean children. The activation of CD14(++) monocyte subsets, which is associated with increased development of atherosclerosis in obese adults, was also readily detected in obese children. Our results indicate that inflammatory mechanisms linking obesity to its metabolic and cardiovascular complications are already activated in childhood obesity.
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