Kim Min Soo, Yan Jingqi, Wu Wenhe, Zhang Guo, Zhang Yalin, Cai Dongsheng
1] Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, USA. [2] Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York, USA. [3] Institute of Aging, Albert Einstein College of Medicine, Bronx, New York, USA.
Nat Immunol. 2015 May;16(5):525-33. doi: 10.1038/ni.3133. Epub 2015 Apr 6.
Innate immunological signals induced by pathogen- and/or damage-associated molecular patterns are essential for adaptive immune responses, but it is unclear if the brain has a role in this process. Here we found that while the abundance of tumor-necrosis factor (TNF) quickly increased in the brain of mice following bacterial infection, intra-brain delivery of TNF mimicked bacterial infection to rapidly increase the number of peripheral lymphocytes, especially in the spleen and fat. Studies of various mouse models revealed that hypothalamic responses to TNF were accountable for this increase in peripheral lymphocytes in response to bacterial infection. Finally, we found that hypothalamic induction of lipolysis mediated the brain's action in promoting this increase in the peripheral adaptive immune response. Thus, the brain-fat axis is important for rapid linkage of innate immunity to adaptive immunity.
由病原体和/或损伤相关分子模式诱导的先天性免疫信号对于适应性免疫反应至关重要，但目前尚不清楚大脑在这一过程中是否发挥作用。我们发现，虽然细菌感染后小鼠大脑中肿瘤坏死因子（TNF）的丰度迅速增加，但脑内注射TNF可模拟细菌感染，迅速增加外周淋巴细胞的数量，尤其是在脾脏和脂肪组织中。对各种小鼠模型的研究表明，下丘脑对TNF的反应是导致细菌感染后外周淋巴细胞增加的原因。最后，我们发现下丘脑诱导的脂肪分解介导了大脑在促进外周适应性免疫反应增加方面的作用。因此，脑-脂肪轴对于先天性免疫与适应性免疫的快速联系至关重要。
