Maldonado-García José Luis, Pérez-Sánchez Gilberto, Becerril Villanueva Enrique, Alvarez-Herrera Samantha, Pavón Lenin, Gutiérrez-Ospina Gabriel, López-Santiago Rubén, Maldonado-Tapia Jesús Octavio, Pérez-Tapia Sonia Mayra, Moreno-Lafont Martha C
Laboratorio de Psicoinmunología, Dirección de Investigaciones en Neurociencias del Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Ciudad de México 14370, Mexico.
Laboratorio de Inmunología Celular, Departamento de Inmunología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Ciudad de México 11340, Mexico.
Microorganisms. 2021 Sep 11;9(9):1937. doi: 10.3390/microorganisms9091937.
Brucellosis is a zoonosis affecting 50,000,000 people annually. Most patients progress to a chronic phase of the disease in which neuropsychiatric symptoms upsurge. The biological processes underlying the progression of these symptoms are yet unclear. Peripheral inflammation mounted against may condition neurochemical shifts and hence unchained neuropsychiatric disorders. Our work aimed at establishing whether neurological, behavioral, and neurochemical disarrays are circumstantially linked to peripheral inflammation uprise secondary to infections. We then evaluated, in control and -infected mice, skeletal muscle strength, movement coordination, and balance and motivation, as well as dopamine, epinephrine, norepinephrine, and serotonin availability in the cerebellum, frontal cortex, and hippocampus. Serum levels of proinflammatory cytokines and corticosterone in vehicle-injected and -infected mice were also estimated. All estimates were gathered at the infection acute and chronic phases. Our results showed that infected mice displayed motor disabilities, muscular weakness, and reduced motivation correlated with neurochemical and peripheral immunological disturbances that tended to decrease after 21 days of infection. The present observations support that disturbed peripheral inflammation and the related neurochemical disruption might lead to mood disorders in infected mice. Future experiments must be aimed at establishing causal links and to explore whether similar concepts might explain neurological and mood disorders in humans affected by brucellosis.
布鲁氏菌病是一种人畜共患病，每年影响5000万人。大多数患者会发展为疾病的慢性阶段，在此阶段神经精神症状会激增。这些症状进展背后的生物学过程尚不清楚。针对[未提及具体病原体]引发的外周炎症可能会导致神经化学变化，进而引发神经精神障碍。我们的研究旨在确定神经、行为和神经化学紊乱是否与继发于[未提及具体病原体]感染的外周炎症加剧有间接关联。然后，我们评估了对照小鼠和感染[未提及具体病原体]的小鼠的骨骼肌力量、运动协调性、平衡和动机，以及小脑、额叶皮质和海马体中多巴胺、肾上腺素、去甲肾上腺素和血清素的可用性。还估计了注射赋形剂的小鼠和感染[未提及具体病原体]的小鼠血清中促炎细胞因子和皮质酮的水平。所有评估均在感染的急性期和慢性期进行。我们的结果表明，感染小鼠表现出运动障碍、肌肉无力和动机降低，这与神经化学和外周免疫紊乱相关，这些紊乱在感染21天后趋于减轻。目前的观察结果支持，外周炎症紊乱和相关的神经化学破坏可能导致感染小鼠出现情绪障碍。未来的实验必须旨在建立因果联系，并探索类似的概念是否可以解释布鲁氏菌病患者的神经和情绪障碍。
