Altered leukocyte distribution under hypercholesterolemia: A cross-sectional study in children with familial

Jacob J Christensen1, Liv T Osnes2, Bente Halvorsen3

  • 1Department of Nutrition, Institute of Basic Medical Sciences, University of Oslo, P.O box 1046, Blindern, 0317 Oslo, Norway; The Lipid Clinic, Oslo University Hospital Rikshospitalet, P.O box 4950, Nydalen, 0424 Oslo, Norway.

Atherosclerosis
|December 27, 2016
PubMed

Insights

Children with familial hypercholesterolemia (FH) show altered monocyte subpopulations, indicating early-stage atherosclerosis. These changes, particularly in those with low HDL cholesterol, suggest monocyte activation in young FH patients.

Area of Science:

  • Immunology
  • Cardiovascular Science
  • Pediatrics

Background:

  • Familial hypercholesterolemia (FH) in children leads to early LDL cholesterol elevation and atherosclerosis.
  • Adult FH patients exhibit pro-inflammatory monocyte phenotypes, but this is unstudied in children.
  • Lymphocyte subpopulation data in FH children is lacking.

Purpose of the Study:

  • To characterize monocyte and lymphocyte subpopulations in children with FH.
  • To compare these subpopulations with healthy children.
  • To investigate early signs of atherosclerosis in FH children.

Main Methods:

  • Flow cytometry was used to analyze B- and T-cell and monocyte subpopulations.
  • Whole blood samples from FH (n=23) and healthy (n=20) children were analyzed.
  • Serum markers of leukocyte and endothelial cell activation were measured via EIA.

Main Results:

  • FH children displayed monocytosis and a shift in monocyte subpopulations.
  • Pro-inflammatory and non-classical monocytes were elevated, while classical monocytes were reduced in FH children.
  • Monocyte changes and elevated CD18/serum E-selectin were prominent in FH children with low HDL cholesterol.

Conclusions:

  • FH children with low HDL cholesterol exhibit monocytosis and a pro-inflammatory monocyte shift.
  • Results suggest monocyte activation occurs at a very early stage of atherosclerosis in humans.
  • This highlights potential early therapeutic targets in pediatric FH.
Abstract

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