Think back to your first ever biology class on mammals. You most likely learned that all mammals, including humans, are warm-blooded (a.k.a., homeotherms) which means that our bodies remain at a constant temperature despite the temperature changes in our environment. So what is it that allows us to maintain this constant body temperature? Answer: thermogenesis.
Thermogenesis, essentially, is the conversion of stored fat into heat (1). We are most familiar with thermogenesis as shivering, which is the (inefficient) conversion of chemical ATP energy into kinetic, then heat energy. For this paper, however, Nguyen, et al. were most interested in non-shivering thermogenesis. The most recent model of thermogenesis dictates that when the hypothalamus senses cold temperatures, it triggers sympathetic discharge, releasing the hormone, noradrenaline, in brown adipose tissue (BAT), and white adipose tissue (WAT) (Fig.1).
Nguyen, et al. found that when mice were exposed to cold temperature, both BAT and WAT activated adipose tissue macrophages that secrete catecholamines, hormones that trigger the fight-or-flight response. However, the effects downstream of catecholamines secretion differ between the two tissue types: catecholamines induce lipolysis in WAT, while in BAT, they induce thermogenic gene expression (4).
Macrophages are like the little ninjas of our immune system—they engulf and kill intracellular pathogen and pathogen components without any particular loyalty to a specific signaling pathway. Given this, they can be activated through two separate pathways: the creatively named classical and alternative activation pathways (3). Our classically activated macrophages, as per their common association, are pro-inflammatory and anti-parasitic in the classical pathway, with the inflammatory antiviral cytokine, IFN-g giving it orders The alternatively activated macrophage, on the other hand, is anti-inflammatory, and pro-survival (Fig. 2). Additionally, alternatively activated macrophages can facilitate wound healing. This pathway does not require priming, like the classical pathway, but often takes its orders from stimuli such as IL-4 and IL-13 (2).
