Adipose tissue recruitment of leukocytes

Abstract

Purpose of Review In December of 2003, two seminal articles describing the presence of macrophages in obese adipose tissue (AT) were published. These AT macrophages (ATMs) are inflammatory and promote local and systemic insulin resistance. Due to the continuing rise in obesity around the world, understanding how these ATMs contribute to metabolic disorders is of much interest. Recent Findings Chemokines have been extensively studied for their role in ATM recruitment. Deficiency or antagonism of chemokine receptors that interact with multiple chemokine ligands reduces ATM accumulation. ATMs are now defined as either classically (M1) or alternatively (M2) activated. PPAR activation and adiponectin promote an M2 polarized state resulting in improved insulin sensitivity. Finally, recent studies have provided evidence that T lymphocytes, NKT cells, mast cells, and B cells also enter AT and may interact with macrophages and adipocytes. Summary Literature published during the past year has shown that macrophage recruitment to AT is only one of the important mediators of obesity-related insulin resistance. The phenotype of ATMs and recruitment of other immune cells to the AT play key roles in the overall contribution of AT to systemic metabolic outcomes of obesity.

Sex differences during the course of diet-induced obesity in mice: adipose tissue expandability and glycemic control

“…These results are supported by the data on DNA concentration in gWAT, namely at week 35. At this time, HF-fed mice showed equal (female mice) or higher (male mice) tissue DNA concentration as compared with the ST-fed mice, in spite of larger adipocytes in the HF-fed animals, in agreement with an increased infiltration of adipose tissue with immune cells in response to HF feeding 22 and with the prominent inflammatory changes occurring in the male mice.…”

“…16 Moreover, larger fat cells are associated with a low-grade adipose tissue inflammation, another key factor linking obesity with insulin resistance. 13,14,[17][18][19] Enhanced secretion of chemoattractants in obese state, like monocyte chemoattractant protein-1 (MCP-1), is believed to promote migration of macrophages 20,21 as well as other immune cells 22 into the tissue accompanied by the phenotypic switch of macrophages to proinflammatory state. 23,24 Higher release of proinflammatory cytokines, like tumor necrosis factor a (TNFa) and interleukin 6, into circulation may disrupt insulin signaling in other tissues.…”

Adipocyte‐derived lipids modulate CD4+ T‐cell function

“…The composition of the SVF varies, depending on the localization of the adipose tissue and the degree of adiposity of the individual, but it typically contains a large variety Correspondence: Dr. Andreea Ioan-Facsinay e-mail: A.Ioan@lumc.nl of cells, including progenitor cells, fibroblasts, endothelial cells, nerve cells, and immune cells. Among the immune cells described in adipose tissue, macrophages and T cells are the most abundant, but other cells, like NK cells, mast cells, and B cells have also been described (reviewed in [1]). While the precise role of these cells in the adipose tissue is largely unknown, there is increasing evidence that cross-talk between immune cells and adipocytes exists and that the immune cells can influence the metabolic functions of the resident adipocytes (reviewed in [1] [2,3], or local differentiation/proliferation of resident T cells [5] under the influence of the adipose tissue environment could constitute underlying mechanisms for changes in the adipose tissue CD4 + T-cell population in obesity.…”

“…Among the immune cells described in adipose tissue, macrophages and T cells are the most abundant, but other cells, like NK cells, mast cells, and B cells have also been described (reviewed in [1]). While the precise role of these cells in the adipose tissue is largely unknown, there is increasing evidence that cross-talk between immune cells and adipocytes exists and that the immune cells can influence the metabolic functions of the resident adipocytes (reviewed in [1] [2,3], or local differentiation/proliferation of resident T cells [5] under the influence of the adipose tissue environment could constitute underlying mechanisms for changes in the adipose tissue CD4 + T-cell population in obesity.Adipose tissue T cells have been previously shown to be present in the vicinity of adipocytes [3]. Moreover, some adipocytederived soluble mediators, such as leptin [10, have been shown to modulate differentiation or cytokine production by CD4 + T cells.…”

MAFB as a novel regulator of human adipose tissue inflammation

“…An important factor regulating changes in metabolism during WAT expansion is an increase in secretion of proinflammatory proteins. An elevated release of monocyte chemoattractant protein 1 (MCP-1; encoded by CCL2) from adipocytes promotes macrophage infiltration of adipose tissue, which further consolidates the inflamed state by releasing a number of proinflammatory peptides [2]. Being a significant constituent of WAT, the macrophage population has gained increased attention as an important modulator of obesitycaused inflammation [3].…”