Department of Neurology, University of Mississippi Medical Center, Jackson, Mississippi, United States.
Department of Cell and Molecular Biology, University of Mississippi Medical Center, Jackson, Mississippi, United States.
Physiol Genomics. 2024 Apr 1;56(4):301-316. doi: 10.1152/physiolgenomics.00113.2023. Epub 2023 Dec 25.
The gut-brain axis interconnects the central nervous system (CNS) and the commensal bacteria of the gastrointestinal tract. The composition of the diet consumed by the host influences the richness of the microbial populations. Traumatic brain injury (TBI) produces profound neurocognitive damage, but it is unknown how diet influences the microbiome following TBI. The present work investigates the impact of a chow diet versus a 60% fat diet (HFD) on fecal microbiome populations in juvenile rats following TBI. Twenty-day-old male rats were placed on one of two diets for 9 days before sustaining either a Sham or TBI via the Closed Head Injury Model of Engineered Rotational Acceleration (CHIMERA). Fecal samples were collected at both 1- and 9-days postinjury. Animals were cognitively assessed in the novel object recognition tests at 8 days postinjury. Fecal microbiota DNA was isolated and sequenced. Twenty days of HFD feeding did not alter body weight, but fat mass was elevated in HFD compared with Chow rats. TBI animals had a greater percentage of entries to the novel object quadrant than Sham counterparts, < 0.05. The Firmicutes/Bacteroidetes ratio was significantly higher in TBI than in the Sham, < 0.05. Microbiota of the Firmicutes lineage exhibited perturbations by both injury and diet that were sustained at both time points. Linear regression analyses were performed to associate bacteria with metabolic and neurocognitive endpoints. For example, counts of were negatively associated with percent entries into the novel object quadrant. Taken together, these data suggest that both diet and injury produce robust shifts in microbiota, which may have long-term implications for chronic health. Traumatic brain injury (TBI) produces memory and learning difficulties. Diet profoundly influences the populations of gut microbiota. Following traumatic brain injury in a pediatric model consuming either a healthy or high-fat diet (HFD), significant shifts in bacterial populations occur, of which, some are associated with diet, whereas others are associated with neurocognitive performance. More work is needed to determine whether these microbes can therapeutically improve learning following trauma to the brain.
肠脑轴将中枢神经系统 (CNS) 和胃肠道的共生细菌相互连接。宿主所消耗的饮食组成会影响微生物群体的丰富度。创伤性脑损伤 (TBI) 会导致严重的神经认知损伤，但尚不清楚饮食如何影响 TBI 后的微生物组。本研究旨在探讨在 TBI 后，幼鼠的普通饮食与高脂肪饮食 (HFD) 对粪便微生物群的影响。20 天大的雄性大鼠在接受闭合性头部损伤的工程旋转加速撞击模型 (CHIMERA) 致伤前 9 天分别接受其中一种饮食，然后进行假手术 (Sham) 或 TBI。在损伤后 1 天和 9 天收集粪便样本。在损伤后 8 天，动物在新颖物体识别测试中进行认知评估。分离并测序粪便微生物 DNA。20 天的 HFD 喂养并未改变体重，但与 Chow 大鼠相比，HFD 喂养的大鼠脂肪量增加。TBI 动物进入新颖物体象限的次数百分比高于 Sham 组，<0.05。与 Sham 相比，TBI 中厚壁菌门/拟杆菌门的比值显著升高，<0.05。Firmicutes 谱系的微生物组受到损伤和饮食的双重影响，并且在两个时间点都持续存在。进行线性回归分析以将细菌与代谢和神经认知终点相关联。例如，数量与进入新颖物体象限的百分比呈负相关。综上所述，这些数据表明，饮食和损伤都会导致微生物组发生强烈变化，这可能对慢性健康产生长期影响。创伤性脑损伤 (TBI) 会导致记忆和学习困难。饮食会极大地影响肠道微生物群的种群。在儿科模型中，无论在 TBI 后摄入健康饮食还是高脂肪饮食 (HFD)，细菌种群都会发生显著变化，其中一些与饮食有关，而另一些与神经认知表现有关。需要进一步研究以确定这些微生物是否可以治疗创伤性脑损伤后的学习障碍。
