ABSTRACT
THEOFILOS POUTAHIDIS, MARKUS KLEINEWIETFELD, CHRISTOPHER SMILLIE, TATIANA LEVKOVICH, ALISON PERROTTA, SIDDHESHVAR BHELA, BERNARD J. VARIAN,YASSIN M. IBRAHIM, JESSICA R. LAKRITZ, SEAN M. KEARNEY, ANTONIS CHATZIGIAGKOS, DAVID A. HAFLER, ERIC J. ALM MAIL, AND SUSAN E. ERDMAN
3.1 INTRODUCTION
The risk of developing obesity rises with a Westernized lifestyle. In industrialized and developing countries obesity contributes to increased mortality by predisposing to serious pathological conditions such as type 2 diabetes, cardiovascular disease, fatty liver, arthritis, asthma, and neoplasia [1]–[2]. Clinical and experimental data suggest that the white adipose tissue of obese organisms is in a low-grade, persistent state of chronic inflammation that exerts adverse systemic effects [2]–[3]. The most prominent inflammatory cell type of the obesity-associated inflammation is the
adipose tissue macrophage. Macrophages are recruited and surround dead adipocytes, thus creating the so-called crown-like structures (CLS). These cells along with hypertrophic adipocytes are thought to be the key cells initiating the unique subclinical pro-inflammatory signaling cascade encountered in obesity [2], [4]–[5]. Macrophages, B and T lymphocytes, and up-regulated pro-inflammatory cytokines including TNF-α, IL-1, IL-6, IL-17, and monocyte chemoattractant protein-1 (MCP-1) have been reported to contribute to obesity-associated pathologies. In parallel, regulatory T cells down-regulate host inflammatory responses [2]–[3], [6]–[10].
