Data on circulating leukocyte subpopulations and inflammatory proteins in children with familial hypercholesterolemia and healthy children

The data in this relies on a previous publication: “Altered leukocyte distribution under hypercholesterolemia: a cross-sectional study in children with familial hypercholesterolemia” (Christensen et al. 2016) [1]. In the present paper, whole blood leukocyte distribution and plasma inflammatory proteins were measured for association with cholesterol concentration and CRP in children with familial hypercholesterolemia (FH) and healthy children.

The data may provide insight on how hypercholesterolemia and inflammation are interconnected in the early phase of atherosclerotic development.
The method can be used for further investigation of cellular or soluble markers of atherosclerosis development in relation to high cholesterol in childhood.

Data
Whole blood leukocyte distribution and plasma level of inflammatory proteins were evaluated for association with cholesterol level and CRP. Data includes correlations between leukocyte subpopulations, cholesterol and CRP in FH children and healthy children combined (Table 1, and Figs. 2 and 3), and comparison of leukocyte distribution in FH children and healthy children less than 13 years of age (Table 2 and Fig. 1).

Experimental design, materials and methods
Data are from cross-sectional study in FH children and healthy children, thoroughly explained elsewhere [1]. Briefly, we recruited children with a definite diagnosis of heterozygous FH from the Lipid Clinic, Oslo University Hospital Rikshospitalet, Oslo, Norway. Control children without FH,  herein referred to as "Healthy children", were recruited in the same time period. For all children, we collected the following: 4 mL heparin plasma for measurement of CRP and lipids, 4 mL EDTA whole blood for characterization of leukocyte subpopulations, and 5 mL serum for analysis of inflammation markers. CRP and lipids were measured using highly standardized protocols at the Department of Medical Biochemistry at Rikshospitalet [1], Oslo, whereas B-and T-cell subpopulations and monocyte subpopulations were analyzed by flow cytometry at the Department of Immunology at Rikshospitalet, Oslo, as described previously [1]. For CRP, lipids and flow cytometry, analyses were performed on the same day as sampling. Serum samples were processed and stored at À 80°C until study completion, followed by measurements of concentration of cluster of differentiation (CD) 163, CD14 and CD25 using enzyme immunoassays from R&D Systems (Minneapolis, MN). Statistical analyses were performed similarly as in [1]. Briefly, the data are presented as mean (standard deviation) or median (25th-75th percentile). Whereas independent samples t-test was used for parametric data, we log-transformed the variables and used independent samples t-test for non-parametric data. Because of skewed distributions, we report Spearman's rank correlation coefficient in the correlation analyses. Alpha level of significance was set to 5%, and SPSS (v22.0, IBM) was used for all calculations.   3. Correlation between pro-inflammatory monocytes and pro-inflammatory lymphocytes. The panels display correlation between pro-inflammatory:classical monocytes ratio and pro-inflammatory CD4þ CD28-lymphocytes in all children (A, n ¼43) and children below 13 years of age (B, n ¼36). r is Spearman's rho (non-parametric) correlation coefficient.

Table 2
Whole blood leukocyte populations characterized by flow cytometry (under the age of 13).

Transparency document. Supplementary material
Transparency document associated with this paper can be found in the online version at http://dx. doi.org/10.1016/j.dib.2016.12.042.