Abstract
Adipose tissue macrophages are a heterogeneous collection of classically activated (M1) and alternatively activated (M2) macrophages. Interleukin 10 (IL-10) is an anti-inflammatory cytokine, secreted by a variety of cell types including M2 macrophages. We generated a macrophage cell line stably overexpressing IL-10 (C2D-IL10) and analyzed the C2D-IL10 cells for several macrophage markers after exposure to adipocytes compared to C2D cells transfected with an empty vector (C2D-vector). C2D-IL10 macrophage cells expressed more CD206 when co-cultured with adipocytes than C2D-vector cells; while the co-cultured cell mixture also expressed higher levels of Il4, Il10, Il1β and Tnf. Since regular C2D cells traffic to adipose tissue after adoptive transfer, we explored the impact of constitutive IL-10 expression on C2D-IL10 macrophages in adipose tissue in vivo. Adipose tissue-isolated C2D-IL10 cells increased the percentage of CD206+, CD301+, CD11c−CD206+ (M2) and CD11c+CD206+ (M1b) on their cell surface, compared to isolated C2D-vector cells. These data suggest that the expression of IL-10 remains stable, alters the C2D-IL10 macrophage cell surface phenotype and may play a role in regulating macrophage interactions with the adipose tissue.
Highlights
Macrophages are a heterogeneous group of cells which have different functions, morphologies and phenotypic properties depending on the microenvironment in which they reside [1,2,3,4,5]
We investigated the impact of constitutive expression of Interleukin 10 (IL-10) on C2D macrophages and how the constitutive expression of IL10 impacts the C2D macrophage phenotype when those macrophages interact with adipocytes in vitro and in vivo
IL-10 is Overexpressed in C2D-IL10 Cells We generated a macrophage cell line that stably expresses IL-10 for use in future studies to determine whether IL-10 could play a role in regulating inflammation in adipose tissue
Summary
Macrophages are a heterogeneous group of cells which have different functions, morphologies and phenotypic properties depending on the microenvironment in which they reside [1,2,3,4,5]. ATMs have been characterized as an anti-inflammatory (M2)-dominant phenotype in lean mice, while there is an increased number of M1-phenotype macrophages in obese subjects [6,8,9,10,13]. It is still unclear if the phenotypic switch of ATMs between M1 and M2 is a consequence of the host having more adipose tissue or if the increased number of M1 cells is an active cause of environmental alteration such as an increased amount of Leptin [14]. Important questions remain about ATM signaling leading to changes in macrophage phenotypes and how this change impacts the adipose tissue microenvironment
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