Evandro J Beraldi, Sukyoung Lee, Yulan Jiang, Isabel M Rea, Rushda Phull, Catherine M Keenan, Matthew Stephens, Martin Bardhi, Oluwamolakun Bankole, Gerald Pfeffer, Jeff Biernaskie, Kathy D McCoy, Eran Elinav, Keith A Sharkey, Minh Dang Nguyen
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引用次数: 0
摘要
肌萎缩性脊髓侧索硬化症(ALS)是人类运动神经元疾病中最常见的一种,其发病较早且以男性为主,但其发病机制却鲜为人知。在这里,我们发现肠道微生物群能抵御 TDP43 的毒性,并导致表达与 ALS 有关的 TDP43 突变形式(A315T)的小鼠出现性二型。在无菌条件下饲养的TDP43小鼠,或用抗生素处理以消耗肠道微生物群的小鼠,会更早出现运动神经元疾病,而且在发病和寿命方面没有性别差异。行为和组织病理学分析证实,肠道微生物群缺失会导致神经退行性病变加剧。阉割不会改变雄性TDP43小鼠的病程,这表明雄性激素不会与肠道微生物群相互作用而导致疾病表型。未来对肠道细菌种类及其作用机制的鉴定将为了解 ALS 的性双态性提供一个独特的机会,其最终目标是开发针对 ALS 的非侵入性和性别特异性治疗方法。
The gut microbiota is a determinant of sexual dimorphism in ALS-linked TDP43 mice
The mechanisms underlying the earlier onset and male predominance of amyotrophic lateral sclerosis (ALS), the most common form of human motoneuron disease, are poorly understood. Here we show that the gut microbiota protects against TDP43 toxicity and contributes to the sexual dimorphism in mice expressing a mutant form of TDP43 (A315T) linked to ALS. TDP43 mice raised under germ-free conditions, or treated with antibiotics to deplete the gut microbiota, develop motoneuron disease earlier and show no sex differences in onset and lifespan. Behavioral and histopathological analyses confirm the exacerbation in neurodegeneration caused by the absence of gut microbiota. Castration did not alter disease course of male TDP43 mice, suggesting that male sex hormones do not interact with the gut microbiota to confer disease phenotype. Future identification of gut bacteria species and their mechanisms of action offers a unique opportunity to understand sexual dimorphism in ALS, with the ultimate goal to develop non-invasive and sex-specific treatments for ALS.