Department of Surgery, and Immunology and Aging Program, The Burn and Shock Trauma Institute, Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA.
Mediators Inflamm. 2010;2010:475139. doi: 10.1155/2010/475139. Epub 2010 Jul 7.
Here, we studied in vitro cytokine production by splenic macrophages obtained from young and aged BALB/c wild type (WT) and IL-6 knockout (IL-6 KO) mice. Relative to macrophages obtained from young WT mice given lipopolysaccharide (LPS), those from aged WT mice had decreased production of proinflammatory cytokines. In contrast, when compared to macrophages from young IL-6 KO mice, LPS stimulation yielded higher levels of these cytokines by cells from aged IL-6 KO mice. Aging or IL-6 deficiency did not affected the percentage of F4/80(+) macrophages, or the surface expression of Toll-like receptor 4 (TLR4) and components of the IL-6 receptor. Overall, our results indicate that IL-6 plays a role in regulating the age-related defects in macrophages through alteration of proinflammatory cytokines, adding to the complexity of IL-6-mediated impairment of immune cell function with increasing age.
在这里，我们研究了从小鼠脾脏巨噬细胞中产生的细胞因子，这些巨噬细胞来自年轻和年老的 BALB/c 野生型（WT）和白细胞介素 6 敲除（IL-6 KO）小鼠。与从小鼠给予脂多糖（LPS）的年轻 WT 小鼠中获得的巨噬细胞相比，来自年老 WT 小鼠的促炎细胞因子的产生减少。相比之下，与从小鼠中获得的 IL-6 KO 年轻小鼠的巨噬细胞相比，LPS 刺激导致来自年老 IL-6 KO 小鼠的细胞产生更高水平的这些细胞因子。衰老或 IL-6 缺乏并不影响 F4/80(+)巨噬细胞的百分比，或 Toll 样受体 4（TLR4）和 IL-6 受体成分的表面表达。总的来说，我们的结果表明，IL-6 通过改变促炎细胞因子在调节巨噬细胞与年龄相关的缺陷方面发挥作用，这增加了随着年龄的增长，IL-6 介导的免疫细胞功能障碍的复杂性。
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