New report, published in Endocrinology, indicates that the sympathetic nerves keep up an anti-anflammatory state in the fat tissue. More specifically, the activity of the sympathetic nervous system (SNS) and its β2-adrenoceptor signaling pathway sustain low levels of the production of the pro-inflammatory cytokine tumor necrosis factor (TNF)-α in macrophages of lean mice.
Pro-inflammatory macrophages play a key role in the pathogenesis of the systemic low-grade chronic inflammation, associated with obesity and insulin resistance (Angela Castoldi et al., Front Immunol, 2016, 6:637).
How resident macrophages’ function is regulated, in lean animals, remains poorly understood. It is known, however that the adipose tissue is heavily innervated by sympathetic/noradrenergic nerves.
The study in Endocrinology by Lijun Tang and colleagues from the National Institute for Physiological Sciences, Okazaki, Aichi, Japan indicates that sympathetic nerves, innervating adipose tissue, down-regulate local TNF-α secretion directly via an effect on β2-adrenoceptors expressed by macrophages. The study also demonstrates that the brain melanocortin pathway is involved in the regulation of the anti-inflammatory state in lean mice via SNS-related mechanisms.
The authors suggest that, in the fat tissue of lean animals, a longstanding suppression of the β-adrenoceptor function may keep the balance of anti-inflammatory versus inflammatory state towards anti-inflammation, and this effect is not related to impairment of thermogenic function.
The sympathetic nerve-immune system interface and the anti-inflammatory SNS impact on macrophages might be dysfunctional in obese animals, and perhaps, in humans with obesity.