Department of Gastroenterology, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Department of Children Rehabilitation Medicine, the Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.
Sci Rep. 2019 Jan 22;9(1):287. doi: 10.1038/s41598-018-36430-z.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder that is characterized by impairments in social interactions and communication, restricted interests and repetitive behaviors. Several studies report a high prevalence of gastrointestinal (GI) symptoms in autistic individuals. Cumulative evidence reveals that the gut microbiota and its metabolites (especially short-chain fatty acids, SCFAs) play an important role in GI disorders and the pathogenesis of ASD. However, the composition of the gut microbiota and its association with fecal SCFAs and GI symptoms of autistic children remain largely unknown. In the present study, we sequenced the bacterial 16S rRNA gene, detected fecal SCFAs, assessed GI symptoms and analyzed the relationship between the gut microbiome and fecal SCFAs in autistic and neurotypical individuals. The results showed that the compositions of the gut microbiota and SCFAs were altered in ASD individuals. We found lower levels of fecal acetic acid and butyrate and a higher level of fecal valeric acid in ASD subjects. We identified decreased abundances of key butyrate-producing taxa (Ruminococcaceae, Eubacterium, Lachnospiraceae and Erysipelotrichaceae) and an increased abundance of valeric acid associated bacteria (Acidobacteria) among autistic individuals. Constipation was the only GI disorder in ASD children in the present study. We also found enriched Fusobacterium, Barnesiella, Coprobacter and valeric acid-associated bacteria (Actinomycetaceae) and reduced butyrate-producing taxa in constipated autistic subjects. It is suggested that the gut microbiota contributes to fecal SCFAs and constipation in autism. Modulating the gut microbiota, especially butyrate-producing bacteria, could be a promising strategy in the search for alternatives for the treatment of autism spectrum disorder.
自闭症谱系障碍（ASD）是一种神经发育障碍，其特征是社交互动和沟通障碍、兴趣受限和重复行为。几项研究报告称，自闭症个体中胃肠道（GI）症状的患病率很高。累积证据表明，肠道微生物群及其代谢物（尤其是短链脂肪酸，SCFAs）在 GI 疾病和 ASD 的发病机制中起重要作用。然而，肠道微生物群的组成及其与自闭症儿童粪便 SCFAs 和 GI 症状的关系在很大程度上仍不清楚。在本研究中，我们对细菌 16S rRNA 基因进行了测序，检测了粪便 SCFAs，评估了 GI 症状，并分析了肠道微生物群与自闭症和神经典型个体粪便 SCFAs 之间的关系。结果表明，自闭症个体的肠道微生物群和 SCFAs 组成发生了改变。我们发现自闭症患者粪便中乙酸和丁酸水平较低，戊酸水平较高。我们发现，与丁酸产生有关的分类群（Ruminococcaceae、Eubacterium、Lachnospiraceae 和 Erysipelotrichaceae）丰度降低，与戊酸有关的细菌（Acidobacteria）丰度增加。在本研究中，自闭症儿童仅存在便秘一种 GI 疾病。我们还发现，在便秘的自闭症患者中，富集了梭菌属、Barnesiella 菌属、粪杆菌属和与戊酸有关的细菌（放线菌科），而丁酸产生菌减少。这表明肠道微生物群有助于自闭症患者粪便中 SCFAs 和便秘。调节肠道微生物群，特别是丁酸产生菌，可能是寻找自闭症谱系障碍治疗替代方法的有前途的策略。
