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The relationship between non-HDL cholesterol and macrophage phenotypes in human adipose tissue

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ABSTRACT

Data from experimental animal models and in vitro studies suggest that both hyperlipoproteinemia and obesity predispose to development of proinflammatory pathways of macrophages within adipose tissue. The aim of this study was to analyze whether non-HDL cholesterol concentration in healthy living kidney donors (LKDs) is related to the number and phenotype of proinflammatory macrophages in visceral and subcutaneous adipose tissue. Adipose tissue samples were collected by cleansing the kidney grafts of LKDs obtained peroperatively. The stromal vascular fractions of these tissues were analyzed by flow cytometry. Proinflammatory macrophages were defined as CD14+ cells coexpressing CD16+ and high-expression CD36 as well (CD14+CD16+CD36+++), while CD16 negativity and CD163 positivity identified alternatively stimulated, anti-inflammatory macrophages. Non-HDL cholesterol concentration positively correlated to proinflammatory macrophages within visceral adipose tissue, with increased strength with more precise phenotype determination. On the contrary, the proportion of alternatively stimulated macrophages correlated negatively with non-HDL cholesterol. The present study suggests a relationship of non-HDL cholesterol concentration to the number and phenotype proportion of macrophages in visceral adipose tissue of healthy humans.

No MeSH data available.


The relations between different macrophage subpopulations and non-HDL cholesterol concentration in visceral adipose tissue. Correlations of macrophage number and proportion of phenotypes with non-HDL cholesterol in the visceral adipose tissue of 47 LKDs (or their subset in E). Consequently, total CD14+ cells (A), CD14+CD16+ cells (B), CD14+CD16+ % (C), CD14+CD16+CD36+++ % (D), CD14+CD16+CD36+++ % (limitation 2–4 mM) (E), and CD14+CD16−CD163+ % (F).
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f2: The relations between different macrophage subpopulations and non-HDL cholesterol concentration in visceral adipose tissue. Correlations of macrophage number and proportion of phenotypes with non-HDL cholesterol in the visceral adipose tissue of 47 LKDs (or their subset in E). Consequently, total CD14+ cells (A), CD14+CD16+ cells (B), CD14+CD16+ % (C), CD14+CD16+CD36+++ % (D), CD14+CD16+CD36+++ % (limitation 2–4 mM) (E), and CD14+CD16−CD163+ % (F).

Mentions: The total number of macrophages per gram of visceral adipose tissue was not significantly related to non-HDL cholesterol in 47 LKDs (Fig. 2A). A borderline level of significance was observed when correlating normally polarized proinflammatory CD16+ macrophage number to non-HDL cholesterol (Fig. 2B). This level of significance substantially increased when expressing the proportion of these macrophages as the percentage of all macrophages in the sample (P < 0.005; Fig. 2C). When including an additional surface marker of the normally polarized macrophages, high CD36 (CD36+++) expression, in the correlation analysis, the correlation of macrophages to non-HDL cholesterol became very close (P < 0.001; Fig. 2D). To determine whether this correlation was expressly produced by the five individuals with the highest concentrations of non-HDL cholesterol, those with levels >4 mM were excluded from the subsequent calculation (Fig. 2E). Although this correlation was limited to individuals within a very narrow range of non-HDL cholesterol between 2 and 4 mM, the significance of the correlation of the proportion of CD16+, CD36+++ to non-HDL cholesterol remained unchanged (P < 0.001). Finally, after calculating the correlation of the proportion of alternatively polarized macrophages to non-HDL cholesterol concentrations, a significant inverse correlation was found (Fig. 2F). All these relationships were also analyzed when the number of macrophages and their proportions were adjusted for sex, age, and BMI. This analysis by multiple linear regression method (JMP 10.0) did not document any effect of these parameters, and the relationship of all macrophage phenotypes to non-HDL cholesterol concentration remained at the same level of significance with the exception of a negative correlation of alternatively stimulated macrophages (CD14+CD16+CD163−; Fig. 2F), where the level of significance was only 0.002 compared with original the 0.0005.


The relationship between non-HDL cholesterol and macrophage phenotypes in human adipose tissue
The relations between different macrophage subpopulations and non-HDL cholesterol concentration in visceral adipose tissue. Correlations of macrophage number and proportion of phenotypes with non-HDL cholesterol in the visceral adipose tissue of 47 LKDs (or their subset in E). Consequently, total CD14+ cells (A), CD14+CD16+ cells (B), CD14+CD16+ % (C), CD14+CD16+CD36+++ % (D), CD14+CD16+CD36+++ % (limitation 2–4 mM) (E), and CD14+CD16−CD163+ % (F).
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC5036370&req=5

f2: The relations between different macrophage subpopulations and non-HDL cholesterol concentration in visceral adipose tissue. Correlations of macrophage number and proportion of phenotypes with non-HDL cholesterol in the visceral adipose tissue of 47 LKDs (or their subset in E). Consequently, total CD14+ cells (A), CD14+CD16+ cells (B), CD14+CD16+ % (C), CD14+CD16+CD36+++ % (D), CD14+CD16+CD36+++ % (limitation 2–4 mM) (E), and CD14+CD16−CD163+ % (F).
Mentions: The total number of macrophages per gram of visceral adipose tissue was not significantly related to non-HDL cholesterol in 47 LKDs (Fig. 2A). A borderline level of significance was observed when correlating normally polarized proinflammatory CD16+ macrophage number to non-HDL cholesterol (Fig. 2B). This level of significance substantially increased when expressing the proportion of these macrophages as the percentage of all macrophages in the sample (P < 0.005; Fig. 2C). When including an additional surface marker of the normally polarized macrophages, high CD36 (CD36+++) expression, in the correlation analysis, the correlation of macrophages to non-HDL cholesterol became very close (P < 0.001; Fig. 2D). To determine whether this correlation was expressly produced by the five individuals with the highest concentrations of non-HDL cholesterol, those with levels >4 mM were excluded from the subsequent calculation (Fig. 2E). Although this correlation was limited to individuals within a very narrow range of non-HDL cholesterol between 2 and 4 mM, the significance of the correlation of the proportion of CD16+, CD36+++ to non-HDL cholesterol remained unchanged (P < 0.001). Finally, after calculating the correlation of the proportion of alternatively polarized macrophages to non-HDL cholesterol concentrations, a significant inverse correlation was found (Fig. 2F). All these relationships were also analyzed when the number of macrophages and their proportions were adjusted for sex, age, and BMI. This analysis by multiple linear regression method (JMP 10.0) did not document any effect of these parameters, and the relationship of all macrophage phenotypes to non-HDL cholesterol concentration remained at the same level of significance with the exception of a negative correlation of alternatively stimulated macrophages (CD14+CD16+CD163−; Fig. 2F), where the level of significance was only 0.002 compared with original the 0.0005.

View Article: PubMed Central - PubMed

ABSTRACT

Data from experimental animal models and in vitro studies suggest that both hyperlipoproteinemia and obesity predispose to development of proinflammatory pathways of macrophages within adipose tissue. The aim of this study was to analyze whether non-HDL cholesterol concentration in healthy living kidney donors (LKDs) is related to the number and phenotype of proinflammatory macrophages in visceral and subcutaneous adipose tissue. Adipose tissue samples were collected by cleansing the kidney grafts of LKDs obtained peroperatively. The stromal vascular fractions of these tissues were analyzed by flow cytometry. Proinflammatory macrophages were defined as CD14+ cells coexpressing CD16+ and high-expression CD36 as well (CD14+CD16+CD36+++), while CD16 negativity and CD163 positivity identified alternatively stimulated, anti-inflammatory macrophages. Non-HDL cholesterol concentration positively correlated to proinflammatory macrophages within visceral adipose tissue, with increased strength with more precise phenotype determination. On the contrary, the proportion of alternatively stimulated macrophages correlated negatively with non-HDL cholesterol. The present study suggests a relationship of non-HDL cholesterol concentration to the number and phenotype proportion of macrophages in visceral adipose tissue of healthy humans.

No MeSH data available.