Zarimeidani Fatemeh, Rahmati Rahem, Mostafavi Mehrnaz, Darvishi Mohammad, Khodadadi Sanaz, Mohammadi Mahya, Shamlou Farid, Bakhtiyari Salar, Alipourfard Iraj
Students Research Committee, Shahrekord University of Medical Sciences, Shahrekord, Iran.
Faculty of Allied Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Inflammation. 2025 Apr;48(2):501-519. doi: 10.1007/s10753-024-02061-y. Epub 2024 Aug 2.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impairments in social communication and behavior, frequently accompanied by restricted and repetitive patterns of interests or activities. The gut microbiota has been implicated in the etiology of ASD due to its impact on the bidirectional communication pathway known as the gut-brain axis. However, the precise involvement of the gut microbiota in the causation of ASD is unclear. This study critically examines recent evidence to rationalize a probable mechanism in which gut microbiota symbiosis can induce neuroinflammation through intermediator cytokines and metabolites. To develop ASD, loss of the integrity of the intestinal barrier, activation of microglia, and dysregulation of neurotransmitters are caused by neural inflammatory factors. It has emphasized the potential role of neuroinflammatory intermediates linked to gut microbiota alterations in individuals with ASD. Specifically, cytokines like brain-derived neurotrophic factor, calprotectin, eotaxin, and some metabolites and microRNAs have been considered etiological biomarkers. We have also overviewed how probiotic trials may be used as a therapeutic strategy in ASD to reestablish a healthy balance in the gut microbiota. Evidence indicates neuroinflammation induced by dysregulated gut microbiota in ASD, yet there is little clarity based on analysis of the circulating immune profile. It deems the repair of microbiota load would lower inflammatory chaos in the GI tract, correct neuroinflammatory mediators, and modulate the neurotransmitters to attenuate autism. The interaction between the gut and the brain, along with alterations in microbiota and neuroinflammatory biomarkers, serves as a foundational background for understanding the etiology, diagnosis, prognosis, and treatment of autism spectrum disorder.
自闭症谱系障碍(ASD)是一种神经发育障碍,其特征是社交沟通和行为受损,常伴有兴趣或活动的受限和重复模式。由于肠道微生物群对称为肠-脑轴的双向通信通路有影响,因此它与ASD的病因有关。然而,肠道微生物群在ASD病因中的具体作用尚不清楚。本研究批判性地审视了最近的证据,以合理化一种可能的机制,即肠道微生物群共生可通过中间细胞因子和代谢产物诱导神经炎症。为了发展为ASD,神经炎症因子会导致肠道屏障完整性丧失、小胶质细胞激活和神经递质失调。它强调了与ASD个体肠道微生物群改变相关的神经炎症中间体的潜在作用。具体而言,诸如脑源性神经营养因子、钙卫蛋白、嗜酸性粒细胞趋化因子等细胞因子以及一些代谢产物和微小RNA被认为是病因生物标志物。我们还概述了益生菌试验如何作为ASD的一种治疗策略,以重新建立肠道微生物群的健康平衡。有证据表明ASD中肠道微生物群失调会诱导神经炎症,但基于循环免疫谱分析的情况尚不清楚。它认为修复微生物群负荷将降低胃肠道的炎症紊乱,纠正神经炎症介质,并调节神经递质以减轻自闭症。肠道与大脑之间的相互作用,以及微生物群和神经炎症生物标志物的改变,是理解自闭症谱系障碍病因、诊断、预后和治疗的基础背景。