Gut Microbiota and Autism Spectrum Disorder: A Neuroinflammatory Mediated Mechanism of Pathogenesis?

IF 4.5 2区 医学 Q2 CELL BIOLOGY
Fatemeh Zarimeidani, Rahem Rahmati, Mehrnaz Mostafavi, Mohammad Darvishi, Sanaz Khodadadi, Mahya Mohammadi, Farid Shamlou, Salar Bakhtiyari, Iraj Alipourfard
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引用次数: 0

Abstract

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.

Abstract Image

肠道微生物群与自闭症谱系障碍:神经炎症介导的发病机制?
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障碍,经常伴有兴趣或活动模式的限制和重复。肠道微生物群被认为与 ASD 的病因有关,因为它影响着被称为 "肠道-大脑轴 "的双向交流途径。然而,肠道微生物群与 ASD 病因的确切关系尚不清楚。本研究对最近的证据进行了批判性研究,以合理解释肠道微生物群共生可通过中间细胞因子和代谢产物诱发神经炎症的可能机制。ASD 的发生需要神经炎症因子导致肠道屏障完整性丧失、小胶质细胞活化和神经递质失调。研究强调了与肠道微生物群改变有关的神经炎症中间产物在 ASD 患者中的潜在作用。具体而言,脑源性神经营养因子、钙黏蛋白、Eotaxin 等细胞因子以及一些代谢物和微RNA 被认为是病因学生物标志物。我们还概述了如何将益生菌试验作为 ASD 的治疗策略,以重建肠道微生物群的健康平衡。有证据表明,在 ASD 中,肠道微生物群失调会诱发神经炎症,但基于循环免疫图谱的分析还不太清楚。它认为,修复微生物群的负荷将降低消化道的炎症混乱,纠正神经炎症介质,调节神经递质,从而减轻自闭症。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,是了解自闭症谱系障碍的病因、诊断、预后和治疗的基础背景。
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来源期刊
Inflammation
Inflammation 医学-免疫学
CiteScore
9.70
自引率
0.00%
发文量
168
审稿时长
3.0 months
期刊介绍: Inflammation publishes the latest international advances in experimental and clinical research on the physiology, biochemistry, cell biology, and pharmacology of inflammation. Contributions include full-length scientific reports, short definitive articles, and papers from meetings and symposia proceedings. The journal''s coverage includes acute and chronic inflammation; mediators of inflammation; mechanisms of tissue injury and cytotoxicity; pharmacology of inflammation; and clinical studies of inflammation and its modification.
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