PDF(Pubmed)
Abstract：
Non-canonical lipolysis induced by inflammatory cytokines or Toll-like receptor ligands is required for the regulation of inflammation during endotoxemia and sepsis. Canonical lipolysis induced by catecholamines declines during aging due to factors including an expansion of lymphocytes, pro-inflammatory macrophage polarization, and an increase in chronic low-grade inflammation; however, the extent to which the non-canonical pathway of lipolysis is active and impacted by immune cells during aging remains unclear. Therefore, we aimed to define the extent to which immune cells from old mice influence non-canonical lipolysis during sepsis. We identified age-associated impairments of non-canonical lipolysis and an accumulation of dysfunctional B1 B cells in the visceral white adipose tissue (vWAT) of old mice. Lifelong deficiency of B cells results in restored non-canonical lipolysis and reductions in pro-inflammatory macrophage populations. Our study suggests that targeting the B cell-macrophage signaling axis may resolve metabolic dysfunction in aged vWAT and attenuate septic severity in older individuals.
摘要：
由炎性细胞因子或Toll样受体配体诱导的非规范脂解是内毒素血症和败血症期间炎症调节所必需的。由于包括淋巴细胞扩增在内的因素，儿茶酚胺诱导的典型脂解在衰老过程中下降，促炎巨噬细胞极化，和慢性低度炎症的增加;然而，在衰老过程中,非经典的脂解途径在多大程度上活跃并受到免疫细胞的影响尚不清楚.因此,我们的目的是确定来自老年小鼠的免疫细胞在脓毒症期间影响非规范脂解的程度.我们确定了老年小鼠内脏白色脂肪组织（vWAT）中非规范脂肪分解和功能失调的B1B细胞积累的年龄相关损伤。B细胞的终身缺乏导致恢复的非规范脂解和促炎巨噬细胞群的减少。我们的研究表明，靶向B细胞-巨噬细胞信号轴可以解决老年vWAT的代谢功能障碍，并减轻老年个体的脓毒症严重程度。
