| Excessive fatty acids and glucose uptake support the infiltration of adipose tissue (AT) by a variety of immune cells including
neutrophils, pro-inflammatory M1 macrophages, and mast cells (MCs). These cells promote inflammation by releasing proinflammatory mediators. The involvement of MCs in AT biology is supported by their accumulation in the AT of obese
individuals along with significantly higher serum levels of MC-derived tryptase. AT-resident MCs under the influence of locally
derived adipokines such as leptin become activated and release pro-inflammatory cytokines including TNFα that worsens the
inflammatory state. MCs support angiogenesis in AT by releasing chymase and inducing preadipocyte differentiation and also the
proliferation of adipocytes through 15-deoxy-delta PGJ2/PPARγ interaction. Additionally, they contribute to the remodeling of
the AT extracellular matrix (ECM) and play a role in the recruitment and activation of leukocytes. MC degranulation has been
linked to brown adipocyte activation, and evidence indicates an important link between MCs and the appearance of BRITE/beige
adipocytes in white AT. Cell crosstalk between MCs and AT-resident cells, mainly adipocytes and immune cells, shows that these
cells play a critical role in the regulation of AT homeostasis and inflammation. |