Isolation on Earth can alter physiology and signaling of organs systems, including the central nervous system. Although not in complete solitude, astronauts operate in an isolated environment during spaceflight. In this study, we determined the effects of isolation and simulated microgravity solely or combined, on the inflammatory cytokine milieu of the hippocampus. Adult female wild-type mice underwent simulated microgravity by hindlimb unloading for 30 days in single or social (paired) housing. In hippocampus, simulated microgravity and isolation each regulate a discrete repertoire of cytokines associated with inflammation. Their combined effects are not additive. A model for mitochondrial reactive oxygen species (ROS) quenching via targeted overexpression of the human catalase gene to the mitochondria (MCAT mice), are protected from isolation- and/or simulated microgravity-induced changes in cytokine expression. These findings suggest a key role for mitochondrial ROS signaling in neuroinflammatory responses to spaceflight and prolonged bedrest, isolation, and confinement on Earth.

地球上的隔离可以改变器官系统的生理和信号，包括中枢神经系统。虽然不是完全孤独，但宇航员在太空飞行期间在一个孤立的环境中工作。在这项研究中，我们单独或联合确定了隔离和模拟微重力对海马体炎症细胞因子环境的影响。成年雌性野生型小鼠在单人或社会（配对）住房中通过后肢卸载进行模拟微重力 30 天。在海马体中，模拟微重力和隔离各自调节与炎症相关的细胞因子的离散库。它们的综合效果不是相加的。线粒体活性氧 (ROS) 通过向线粒体（MCAT 小鼠）靶向过度表达人过氧化氢酶基因而淬灭的模型，免受隔离和/或模拟微重力诱导的细胞因子表达变化。这些发现表明线粒体 ROS 信号在对太空飞行和地球上长期卧床休息、隔离和限制的神经炎症反应中起着关键作用。