Proinflammatory alterations of white adipose tissue (WAT) with increasing age play an important role in mammalian aging. WAT produced eotaxin-1 (CCL11—C-C motif chemokine ligand 11) and monocyte chemoattractant protein 1 (MCP-1) (CCL2) are elevated in old mammals. Obese and old adipose tissues produce excessive proinflammatory cytokines such as interleukin (IL)-6, CCL2, and IL-1-beta that contribute to inflammaging. WAT-based inflammaging involves an altered homeostatic equilibrium between proinflammatory cells such as activated type 1 macrophages, B cells (high IgJ) and T cells, and anti-inflammatory eosinophils and Tregs. Specifically, young and lean individuals exhibit a high eosinophil-to-macrophage ratio with an enrichment of alternative activated tissue macrophages that is reduced in the WAT of aging mice. Eosinophils from young animals adoptively transferred to old mice, home to WAT and reverse many of the immunoinflammatory signatures associated with aging. Whether eosinophil-based therapies for inflammaging could be created remains an open question.

中文翻译：

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嗜酸性粒细胞和白色脂肪：防止蠕虫和发炎。

随着年龄的增长，白色脂肪组织（WAT）的促炎性变化在哺乳动物衰老中起重要作用。WAT产生的嗜酸性粒细胞趋化因子-1（CCL11-CC趋化因子配体11）和单核细胞趋化蛋白1（MCP-1）（CCL2）在老年哺乳动物中升高。肥胖和老旧的脂肪组织会产生过多的促炎细胞因子，例如白细胞介素（IL）-6，CCL2和IL-1-beta，从而引起发炎。基于WAT的发炎涉及促炎细胞（如活化的1型巨噬细胞，B细胞（高IgJ）和T细胞）与抗炎嗜酸性粒细胞和Tregs之间的稳态平衡变化。具体而言，年轻和瘦弱的个体表现出高的嗜酸性粒细胞与巨噬细胞比率，并具有在衰老小鼠的WAT中减少的替代活化组织巨噬细胞的富集。来自幼小动物的嗜酸性粒细胞过继地转移到WAT所在的老年小鼠中，并逆转了许多与衰老相关的免疫炎症特征。是否可以建立基于嗜酸性粒细胞的发炎疗法仍然是一个悬而未决的问题。