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 pro-inflammatory 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.

中文翻译：

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生理和病理条件下肥大细胞与脂肪细胞之间的串扰。

过多的脂肪酸和葡萄糖摄取会支持各种免疫细胞（包括嗜中性粒细胞，促炎性M1巨噬细胞和肥大细胞（MC））渗入脂肪组织（AT）。这些细胞通过释放促炎介质来促进炎症。MCs参与AT生物学的研究得到了它们在肥胖个体AT中的积累以及血清中MC衍生的类胰蛋白酶的明显升高的支持。在本地衍生的脂肪因子如瘦素的作用下，驻留于AT的MCs被激活并释放促炎细胞因子，包括恶化炎症状态的TNFα。MC通过释放糜酶和诱导前脂肪细胞分化以及通过15-脱氧-δPGJ2 /PPARγ相互作用来促进脂肪细胞的增殖来支持AT中的血管生成。另外，它们有助于AT细胞外基质（ECM）的重塑，并在白细胞的募集和激活中发挥作用。MC脱粒与棕色脂肪细胞的活化有关，证据表明MC与白色AT中BRITE /米色脂肪细胞的出现之间有重要的联系。MC与AT驻留细胞（主要是脂肪细胞和免疫细胞）之间的细胞串扰表明，这些细胞在调节AT稳态和炎症中起关键作用。