Souza Vanessa da Silva, Manhães-de-Castro Raul, Pereira Sabrina da Conceição, de Silveira Beatriz Souza, Calado Caio Matheus Santos da Silva, Gouveia Henrique José Cavalcanti Bezerra, Coq Jacques-Olivier, Toscano Ana Elisa
Graduate Program in Neuropsychiatry and Behavioral Sciences, Center for Medical Sciences, Federal University of Pernambuco, Recife 50670-901, Pernambuco, Brazil.
Studies in Nutrition and Phenotypic Plasticity Unit, Center for Health Sciences, Federal University of Pernambuco, Recife 50670-420, Pernambuco, Brazil.
Cells. 2025 Jul 11;14(14):1063. doi: 10.3390/cells14141063.
Early-life brain injuries are major causes of long-term neurodevelopmental disorders such as cerebral palsy. Emerging evidence suggests these injuries can alter the gut microbiota composition, intestinal integrity, and neuroinflammatory responses. This systematic review evaluated the impact of early-life brain injuries on the gut microbiota in rodent models. A scientific literature search was conducted across Medline/PubMed, Web of Science, Scopus, and Embase. Initially, 7419 records were identified, and 21 eligible studies were included. Eligible studies focused on evaluating the microbiota alterations and related gut-brain axis markers at the neonatal or post-weaning stages. The data extraction and synthesis followed PRISMA guidelines. Most studies reported gut dysbiosis characterized by a decreased abundance of Bacteroidetes, and . Alterations were associated with an increased gut permeability, reduced tight junction proteins, and elevated pro-inflammatory cytokines. Several studies showed reduced levels of short-chain fatty acids and metabolic pathway disruptions. Brain outcomes included neuroinflammation, white matter injury, altered gene expression, and impaired structural integrity. These results suggest that early-life brain injury induces complex alterations in the gut microbiota and its metabolic products, which may contribute to systemic and neuroinflammatory processes. Understanding these interactions offers insights into the pathophysiology of neurodevelopmental disorders and highlights the gut-brain axis as a potential target for early interventions.
早期脑损伤是导致脑瘫等长期神经发育障碍的主要原因。新出现的证据表明，这些损伤会改变肠道微生物群组成、肠道完整性和神经炎症反应。本系统评价评估了啮齿动物模型中早期脑损伤对肠道微生物群的影响。通过检索Medline/PubMed、科学网、Scopus和Embase进行科学文献检索。最初，共识别出7419条记录，纳入了21项符合条件的研究。符合条件的研究重点评估新生儿期或断奶后阶段的微生物群改变及相关的肠-脑轴标志物。数据提取和综合遵循PRISMA指南。大多数研究报告称肠道微生物群失调的特征是拟杆菌丰度降低。这些改变与肠道通透性增加、紧密连接蛋白减少和促炎细胞因子升高有关。多项研究显示短链脂肪酸水平降低和代谢途径紊乱。脑部结果包括神经炎症、白质损伤、基因表达改变和结构完整性受损。这些结果表明，早期脑损伤会引起肠道微生物群及其代谢产物的复杂改变，这可能会导致全身和神经炎症过程。了解这些相互作用有助于深入了解神经发育障碍的病理生理学，并突出肠-脑轴作为早期干预潜在靶点的重要性。
