Arenas-Mosquera D, Cerny N, Cangelosi A, Geoghegan P A, Malchiodi E L, De Marzi M, Pinto A, Goldstein J
Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Instituto de Fisiología y Biofísica ''Houssay" (IFIBIO), Laboratorio de Neurofisiopatología, Facultad de Medicina, Paraguay 2155 Piso 7, 1121, Ciudad de Buenos Aires, Argentina.
Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Cátedra de Inmunología e Instituto de Estudios de La Inmunidad Humoral (IDEHU), UBA-CONICET, Junín 956 Piso 4, 1113, Ciudad de Buenos Aires, Argentina.
Heliyon. 2024 Oct 26;10(21):e39871. doi: 10.1016/j.heliyon.2024.e39871. eCollection 2024 Nov 15.
Nutrition quality could be one of the reasons why, in the face of a Shiga toxin-producing enterohemorrhagic outbreak, some patients experience more profound deleterious effects than others, including unfortunate deaths. Thus, the aim of this study was to determine whether high-fat and/or high-carbohydrate diets could negatively modulate the deleterious action of Shiga toxin 2 on ventral anterior and ventral lateral thalamic nuclei and the internal capsule, the neurological centers responsible for motor activity.
Mice were fed a regular, high-fat, high-carbohydrate diet or a combination of both previous to the intravenous administration of Shiga toxin 2 or vehicle. Four days after intravenous administration, mice were subjected to behavioral tests and then sacrificed for histological and immunofluorescence assays to determine alterations in the neurovascular unit at the cellular and functional levels. Statistical analysis was performed using one-way analysis of variance followed by Bonferroni test. The criterion for significance was p = 0.0001 for all experiments.
The high-fat and the high-carbohydrate diets significantly heightened the deleterious effect of Stx2, while the combination of both diets yielded the worst results, including endothelial glycocalyx and oligodendrocyte alterations, astrocyte and microglial reactivity, neurodegeneration, and motor and sensitivity impairment.
In view of the results presented here, poor nutrition could negatively influence patients affected by Stx2 at a neurological level. Systemic effects, however, cannot be ruled out.
营养质量可能是在产志贺毒素的肠出血性大肠杆菌爆发时,一些患者比其他患者出现更严重有害影响(包括不幸死亡)的原因之一。因此,本研究的目的是确定高脂肪和/或高碳水化合物饮食是否会对志贺毒素2对腹前核、腹外侧丘脑核和内囊(负责运动活动的神经中枢)的有害作用产生负面影响。
在静脉注射志贺毒素2或赋形剂之前,给小鼠喂食常规、高脂肪、高碳水化合物饮食或两者的组合。静脉注射四天后,对小鼠进行行为测试,然后处死以进行组织学和免疫荧光分析,以确定神经血管单元在细胞和功能水平上的改变。使用单因素方差分析,随后进行Bonferroni检验进行统计分析。所有实验的显著性标准为p = 0.0001。
高脂肪和高碳水化合物饮食显著增强了志贺毒素2的有害作用,而两种饮食的组合产生了最糟糕的结果,包括内皮糖萼和少突胶质细胞改变、星形胶质细胞和小胶质细胞反应性、神经变性以及运动和感觉障碍。
鉴于此处呈现的结果,营养不良可能会在神经水平上对受志贺毒素2影响的患者产生负面影响。然而,不能排除全身影响。