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首页> 外文期刊>The journals of gerontology.Series A. Biological sciences and medical sciences >Age-Associated Increase in Cytokine Production During Systemic Inflammation-II: The Role of IL-1 beta in Age-Dependent IL-6 Upregulation in Adipose Tissue
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Age-Associated Increase in Cytokine Production During Systemic Inflammation-II: The Role of IL-1 beta in Age-Dependent IL-6 Upregulation in Adipose Tissue

机译：与年龄相关的全身性炎症期间细胞因子生产的增加-II：IL-1β在脂肪组织中年龄依赖性IL-6上调中的作用

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摘要

Expression of interleukin-6 (IL-6) upon acute inflammatory stress is significantly augmented by aging in adipose tissue, a major source of this cytokine. In the present study, we examined the mechanism of age-dependent IL-6 overproduction using visceral white adipose tissue from C57BL/6 mice. Upon treatment with lipopolysaccharide (LPS) in vitro, IL-6 was produced by adipose tissue explants, and secreted levels were significantly higher in cultures from aged (24 months) mice compared to young (4 months). Interleukin 1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha), two inducers of IL-6, were mainly produced by the lungs and spleen rather than adipose tissue in mice after LPS injection. Treatment of adipose explants with physiological levels of IL-1 beta induced significant age-dependent secretion of IL-6, while treatment with TNF alpha had little effect, demonstrating an augmented response of adipose tissues to IL-1 beta in the aged. In vitro experiments utilizing a neutralizing antibody against IL-1 beta and in vivo experiments utilizing IL-1-receptor-1 deficient mice, confirmed that IL-6 overproduction in the aged is regulated by autocrine/paracrine action of IL-1 beta which specifically occurs in aged adipose tissues. These findings indicate an elevated inflammatory potential of adipose tissue in the aged and a unique IL-1 beta-mediated mechanism for IL-6 overproduction, which may impact age-associated vulnerability to acute inflammatory diseases such as sepsis.
机译：脂肪组织老化是该细胞因子的主要来源，急性炎症应激时白细胞介素6（IL-6）的表达显着增强。在本研究中，我们使用来自C57BL / 6小鼠的内脏白色脂肪组织检查了年龄依赖性IL-6过度生产的机制。在体外用脂多糖（LPS）处理后，脂肪组织外植体会产生IL-6，与年幼（4个月）相比，年龄（24个月）小鼠的培养物中分泌水平显着更高。 ILPS的两种诱导物白介素1 beta（IL-1 beta）和肿瘤坏死因子α（TNF alpha）主要是由LPS注射后小鼠的肺和脾脏而非脂肪组织产生的。用生理水平的IL-1β处理脂肪外植体可诱导显着的年龄依赖性IL-6分泌，而用TNFα治疗几乎没有作用，这表明老年人中脂肪组织对IL-1β的反应增强。利用针对IL-1β的中和性抗体的体外实验和利用IL-1受体1缺陷型小鼠的体内实验，证实了老年人中IL-6的过量生产受IL-1β的自分泌/旁分泌作用所调节。发生在老化的脂肪组织中。这些发现表明，老年人中脂肪组织的炎性潜能增加，并且IL-1β介导的IL-6过量产生的独特机制可能影响与年龄相关的易感性疾病，如败血症。

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