Clinical Features and Gut Microbial Alterations in Anti-leucine-rich Glioma-Inactivated 1 Encephalitis-A Pilot Study.
Clinical Features and Gut Microbial Alterations in Anti-leucine-rich Glioma-Inactivated 1 Encephalitis-A Pilot Study.
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富含抗达蛋白的神经胶质瘤灭活1脑炎的临床特征和肠道微生物改变。
DOI：
10.3389/fneur.2020.585977
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发表时间：
2020
影响因子：
3.4
通讯作者：
Chen X
中科院分区：
文献类型：
--
作者：
Ma X;Ma L;Wang Z;Liu Y;Long L;Ma X;Chen H;Chen Z;Lin X;Si L;Chen X
抗富含亮氨酸的胶质瘤失活1（抗LGI1）脑炎是一种罕见的自身免疫性脑炎（AE）。我们调查了抗LGI1脑炎的临床特征和肠道微生物的变化。在免疫治疗之前，在研究中招募了15名新诊断为抗LGI1脑炎的患者。对照组包括25名匹配良好的健康对照（HC）。所有参与者都是来自中国南方的汉族人。收集患者的临床资料和粪便标本。通过16S核糖体RNA（16S rRNA）基因测序分析肠道菌群的多样性和组成。结果表明，抗LGI1脑炎的特征是认知障碍，面臂张力障碍性癫痫发作，低钠血症和精神症状。脑电图异常9例，脑MRI异常10例。与HC相比，抗LGI1脑炎患者表现出微生物多样性减少和肠道微生物组整体组成改变。在门水平上，抗LGI1脑炎患者表现出较高丰度的变形菌门和较低丰度的厚壁菌门。门水平的改变与自身免疫性和炎症性疾病有关。在属的水平上，鞘氨醇单胞菌属、厌氧菌属、琥珀弧菌属、梭菌属和SMB53（与运动障碍、精神疾病和促炎作用相关的属）的数量增加。然而，在患者组中，粪杆菌属、罗斯拜瑞氏菌属、毛螺菌属、瘤胃球菌属和布劳特氏菌属[能够产生短链脂肪酸（SCFA）的属]明显减少。我们的研究结果表明，抗LGI1脑炎的特点是特殊的临床特征，并伴随着特定的肠道微生物群的改变。由于样本量有限且不适用于其他人群，需要进一步研究以探索肠道微生物群与抗LGI1脑炎之间的关系。
Anti-leucine-rich glioma-inactivated 1 (anti-LGI1) encephalitis is a rare autoimmune encephalitis (AE). We investigated the clinical features and gut microbial alterations of anti-LGI1 encephalitis. Fifteen patients newly diagnosed with anti-LGI1 encephalitis were recruited in the study prior to the administration of immunotherapy. The control group contains 25 well-matched healthy controls (HCs). All participants were Han Chinese from South China. Their clinical data and fecal samples were collected. The diversity and composition of gut microbiota were analyzed by 16S ribosomal RNA (16S rRNA) gene sequencing. The results showed that anti-LGI1 encephalitis was characterized by cognitive impairment, faciobrachial dystonic seizures, hyponatremia, and psychiatric symptoms. Abnormal EEG and brain MRI were presented in 9 and 10 patients, respectively. Compared to HCs, the anti-LGI1 encephalitis patients exhibited a decreased microbial diversity and an altered overall composition of gut microbiome. At the phylum level, anti-LGI1 encephalitis patients exhibited a higher abundance of Proteobacteria and a lower abundance of Firmicutes. The alterations in the phylum level were associated with autoimmune and inflammatory disorders. At the genus level, there was an increase in Sphingomonas, Anaerofustis, Succinvibrio, Clostridium, and SMB53 (genera related to movement disorders, psychiatric diseases, and with proinflammatory effects). However, the Faecalibacterium, Roseburia, Lachnospira, Ruminococcus, and Blautia [genera with ability to produce short-chain fatty acids (SCFAs)] were obviously reduced in the patient group. Our results suggest that anti-LGI1 encephalitis is characterized by special clinical features and is accompanied by alterations in specific gut microbiota. For the limited sample size and non-applicability to other populations, further studies are warranted to explore the relationships between gut microbiota and anti-LGI1 encephalitis.
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