Brain and behavior · 2026
Identifying Immune Cells as Mediators in the Impact of Gut Microbiota on Congenital Malformations of the Nervous System.
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Tian Haokun, Guo Xiaolan, Yu Jialu, Lu Yuanfang, Cao Wensen, Wang Xiuwei, Zhu Zhiqiang, Guan Zhen, Yang Aiyun, Li Shen, Xu Xiaochun, Wang Caihua, Wang Jianhua
Аннотация
INTRODUCTION: Congenital malformations of the nervous system, such as neural tube defects, are significant contributors to infant morbidity and mortality. This study aimed to assess the causal influence of gut microbiota on nervous system malformations and to identify immune cells as potential mediators in this relationship, utilizing a two-step Mendelian randomization (TSMR) approach.
METHODS: Using genome-wide association studies data on gut microbiota, immune cells, and congenital malformations of the nervous system, we applied TSMR to evaluate the total, direct, and mediating effects. Gut microbiota indicators served as exposures, congenital malformations of the nervous system as outcomes, and immune cell markers as mediators. Statistical analyses included MR Egger, inverse variance weighted, and so forth.
RESULTS: Our analysis identified 19 gut microbiota indicators causally associated with congenital malformations of the nervous system. Notably, Eubacteriaceae and Eubacterium genera exhibited protective effects, while Escherichia and Bacteroides genera showed positive correlations with malformation risk. Nine immune cell indicators significantly mediated these effects. For example, CD20+ B cells were negatively associated with malformation risk, suggesting a protective immune response, whereas CD25+ B cells were positively correlated, indicating increased malformation risk.
CONCLUSIONS: This study demonstrated a significant link between gut microbiota composition and congenital nervous system malformations, mediated by specific immune cells. These findings highlighted the potential for gut microbiota modulation and immune-targeted therapies as preventive or therapeutic strategies in reducing malformation risks. Future investigations should aim to replicate these results across diverse populations and further elucidate the underlying biological mechanisms of gut-immune-neural interactions.
TRIAL REGISTRATION: The authors have nothing to report.
METHODS: Using genome-wide association studies data on gut microbiota, immune cells, and congenital malformations of the nervous system, we applied TSMR to evaluate the total, direct, and mediating effects. Gut microbiota indicators served as exposures, congenital malformations of the nervous system as outcomes, and immune cell markers as mediators. Statistical analyses included MR Egger, inverse variance weighted, and so forth.
RESULTS: Our analysis identified 19 gut microbiota indicators causally associated with congenital malformations of the nervous system. Notably, Eubacteriaceae and Eubacterium genera exhibited protective effects, while Escherichia and Bacteroides genera showed positive correlations with malformation risk. Nine immune cell indicators significantly mediated these effects. For example, CD20+ B cells were negatively associated with malformation risk, suggesting a protective immune response, whereas CD25+ B cells were positively correlated, indicating increased malformation risk.
CONCLUSIONS: This study demonstrated a significant link between gut microbiota composition and congenital nervous system malformations, mediated by specific immune cells. These findings highlighted the potential for gut microbiota modulation and immune-targeted therapies as preventive or therapeutic strategies in reducing malformation risks. Future investigations should aim to replicate these results across diverse populations and further elucidate the underlying biological mechanisms of gut-immune-neural interactions.
TRIAL REGISTRATION: The authors have nothing to report.