这项研究旨在调查自闭症谱系障碍(ASD)儿童与神经典型(NT)儿童相比的肠道菌群组成。重点是确定这些群体之间肠道细菌的潜在差异。通过16SRNA基因V3-V4区域的大规模测序分析微生物群,利用从参与者粪便样本中提取的DNA。我们的发现表明,优势细菌门(Firmicutes,拟杆菌,放线菌,变形杆菌,野生微生物群)在ASD和NT组之间。然而,在属一级,在布劳蒂亚的丰度上观察到显著的差异,普雷沃氏菌,十一梭菌,和梭状芽孢杆菌XVIII,所有这些以前都与ASD有关。此外,一项基于性别的分析揭示了肠道微生物群组成的额外差异.具体来说,三个属(Megamonas,镰刀菌,酸性细菌球菌)在ASD和NT队列中的男性和女性群体之间表现出差异。特别值得注意的是Megamonas在ASD女性中的独家存在。预测的代谢途径的分析表明与胺和多胺降解相关的途径的富集,以及ASD组中的氨基酸降解。相反,与碳水化合物生物合成有关的途径,降解,发酵被发现代表性不足。尽管我们的研究有局限性,包括相对较小的样本量(30个ASD和31个NT儿童)和利用来自16SRNA基因分析而不是宏基因组测序的预测代谢途径,我们的发现有助于越来越多的证据表明肠道微生物群组成与ASD之间存在潜在关联.未来的研究工作应该集中在用更大的样本量来验证这些发现,并探索ASD中这些微生物差异的功能意义。此外,迫切需要进一步研究以阐明肠道菌群组成的性别差异及其对ASD病理和治疗的潜在影响.
This study aimed to investigate the gut microbiota composition in children with autism spectrum disorder (ASD) compared to neurotypical (NT) children, with a focus on identifying potential differences in gut bacteria between these groups. The microbiota was analyzed through the massive sequencing of region V3-V4 of the 16S RNA gene, utilizing DNA extracted from stool samples of participants. Our findings revealed no significant differences in the dominant bacterial phyla (Firmicutes, Bacteroidota, Actinobacteria, Proteobacteria, Verrucomicrobiota) between the ASD and NT groups. However, at the genus level, notable disparities were observed in the abundance of Blautia, Prevotella, Clostridium XI, and Clostridium XVIII, all of which have been previously associated with ASD. Furthermore, a sex-based analysis unveiled additional discrepancies in gut microbiota composition. Specifically, three genera (Megamonas, Oscilibacter, Acidaminococcus) exhibited variations between male and female groups in both ASD and NT cohorts. Particularly noteworthy was the exclusive presence of Megamonas in females with ASD. Analysis of predicted metabolic pathways suggested an enrichment of pathways related to amine and polyamine degradation, as well as amino acid degradation in the ASD group. Conversely, pathways implicated in carbohydrate biosynthesis, degradation, and fermentation were found to be underrepresented. Despite the limitations of our study, including a relatively small sample size (30 ASD and 31 NT children) and the utilization of predicted metabolic pathways derived from 16S RNA gene analysis rather than metagenome sequencing, our findings contribute to the growing body of evidence suggesting a potential association between gut microbiota composition and ASD. Future research endeavors should focus on validating these findings with larger sample sizes and exploring the functional significance of these microbial differences in ASD. Additionally, there is a critical need for further investigations to elucidate sex differences in gut microbiota composition and their potential implications for ASD pathology and treatment.