Endogenous, adipocyte-derived lipids signal the recruitment of proinflammatory immune cells.

Abstract

Obesity, insulin resistance, and type 2 diabetes have reached epidemic levels in Western countries. Work over the past decade has established that the adipose tissue in obesity is characterized by a state of chronic, low-grade inflammation, which plays a primary role in the development of systemic insulin resistance (1). Critical to the development of adipose tissue inflammation in obesity is the recruitment of specific immune cells, such as proinflammatory macrophages (M1 macrophages) and neutrophils (1–3). However, the precise signals that stimulate the recruitment of these immune cells into the expanding adipose tissue are not well understood. In this issue, Tynan et al. (4) demonstrate that endogenous oils (EOs) isolated from human adipocytes are a potent inflammatory signal. Initially, the authors sought to determine whether EOs derived from human omental adipocytes could enhance antigen-specific immune responses in mice. Remarkably, EOs were as effective as incomplete Freund’s adjuvant at inducing antigen-specific antibody responses. Importantly, fractionation of EOs into lipid and nonlipid components demonstrated that the lipid fraction of EOs were the immunogenic component. To explore their inflammatory properties further, the authors used a model of inflammation in which the recruitment of immune cells was examined following the injection of EOs into the peritoneum of mice. EOs induced a marked shift in the immune cell profile of the peritoneum, characterized by …