Crosstalk between brown adipocytes and macrophages

There are two types of adipose tissue (AT): white adipose tissue (WAT), which is involved in energy storage, and brown adipose tissue (BAT) that dissipates energy in the form of heat (non‐shivering‐thermogenesis). AT acts as an endocrine organ that secretes hormones or cytokines known as adipokines. Dysregulation of secretion of adipokines, caused by adipocyte hypertrophy and dysfunction, is directly linked to chronic inflammation. Inflammation of WAT during obesity leads to increased expression and secretion of pro‐inflammatory cytokines such as TNF‐α, IL‐6, MCP‐1 (Villarroya et al., 2018). This increase in adipocyte‐derived pro‐inflammatory cytokines causes a dramatic shift in the immune cell population, especially in macrophages, and leads to metaflammation. On the other hand, adipose tissue‐resident macrophages (ATMs) play a very important role in innervation and energy expenditure of BAT (Wolf et al., 2017). All these facts are the reason why we investigate signal pathways as well as secreted molecules that play a role in the communication between brown adipocytes and ATM. We are focusing on the crosstalk between brown adipocytes and macrophages. We used three in vitro models: direct co‐cultivation, transwell system and conditioned medium. In our experiments, we used two different types of macrophages: fetal liver derived macrophages (FLDMs) and bone marrow derived macrophages (BMDMs). We found that macrophages regulate expression of adipogenic (e.g. PPARg) as well as thermogenic (e.g. UCP1) markers. Interestingly, we observed that brown adipocytes produce different factors that regulate macrophages and their pro‐ versus anti‐inflammatory phenotype. These data indicate a crosstalk between macrophages and adipocytes in BAT. Support or Funding Information Institute of Pharmacology and Toxicology, University of Bonn, 53127 Bonn, Germany Research Training Group 1873, University of Bonn, 53127 Bonn, Germany