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How the brain regulates inflammation
Nature Reviews Immunology ( IF 100.3 ) Pub Date : 2024-05-14 , DOI: 10.1038/s41577-024-01045-1
Alexandra Flemming

Infections can activate neural circuits that mediate responses such as fever and malaise. Jin et al. describe a body-to-brain neural circuit that informs the brain of emerging inflammatory responses. Intraperitoneal injection of mice with lipopolysaccharide (LPS) or other immune insults was shown to activate specific neurons in the caudal nucleus of the solitary tract (cNST) in the brainstem. Genetic silencing of these neurons resulted in out-of-control inflammatory responses to LPS challenge, whereas their activation reduced levels of pro-inflammatory cytokines and activated anti-inflammatory responses. The authors found that anti-inflammatory and pro-inflammatory cytokines activate two different populations of vagal neurons that transmit inflammatory information to the cNST neurons. Chemogenetic activation of these circuits dramatically increased survival of mice in response to lethal LPS challenge and protected mice in models of ulcerative colitis. In mice infected with Salmonella, it led to significantly increased bacterial loads. These results highlight the central role of this body-to-brain anti-inflammatory circuit in immune regulation and suggest that its pharmacological targeting may help to manage immune disorders.



中文翻译:

大脑如何调节炎症

感染可以激活神经回路,介导发烧和不适等反应。金等人。描述了一种身体到大脑的神经回路,该回路向大脑通报正在出现的炎症反应。小鼠腹腔注射脂多糖(LPS)或其他免疫刺激物被证明可以激活脑干孤束尾核(cNST)中的特定神经元。这些神经元的基因沉默导致对脂多糖攻击的炎症反应失控,而它们的激活降低了促炎细胞因子的水平并激活了抗炎反应。作者发现抗炎和促炎细胞因子激活两种不同的迷走神经元群,将炎症信息传递到 cNST 神经元。这些回路的化学遗传学激活显着提高了小鼠对致命性 LPS 攻击的存活率,并在溃疡性结肠炎模型中保护了小鼠。在感染沙门氏菌的小鼠中,它导致细菌负荷显着增加。这些结果强调了这种从身体到大脑的抗炎回路在免疫调节中的核心作用,并表明其药理学靶向可能有助于控制免疫紊乱。

更新日期:2024-05-14
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