Autonomic Nervous System Neuroanatomical Alterations Could Provoke and Maintain Gastrointestinal Dysbiosis in Autism Spectrum Disorder (ASD): A Novel Microbiome-Host Interaction Mechanistic Hypothesis.
Autonomic Nervous System Neuroanatomical Alterations Could Provoke and Maintain Gastrointestinal Dysbiosis in Autism Spectrum Disorder (ASD): A Novel Microbiome-Host Interaction Mechanistic Hypothesis.
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自主神经系统神经解剖学改变可能引发并维持自闭症谱系障碍 (ASD) 的胃肠道生态失调：一种新的微生物组-宿主相互作用机制假设。
DOI：
10.3390/nu14010065
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发表时间：
2021-12-24
期刊：
影响因子：
5.9
通讯作者：
Iris F
中科院分区：
文献类型：
--
作者：
Beopoulos A;Gea M;Fasano A;Iris F
继发于环境因素（包括饮食模式、抗生素使用、污染暴露和其他生活方式因素）的菌群失调与许多非感染性慢性炎症性疾病有关。自闭症谱系障碍 (ASD) 与母体炎症有关，尽管没有确凿的证据表明受影响的个体患有许多心理和精神疾病中的全身性低度炎症。然而，在自闭症谱系障碍患者中观察到神经炎症和神经免疫异常。通过重新平衡人类肠道微生物群来治疗疾病已被广泛研究，但结果尚无定论且相互矛盾。这些观察结果强烈表明，自闭症谱系障碍 (ASD) 患者所遇到的生态失调也可能源于自主神经系统 (ANS) 功能异常，这是自闭症谱系障碍 (ASD) 的常见神经解剖学改变。根据这一假设，由于自闭症谱系障碍（ASD）特异性副交感神经活动缺陷，ANS 交感神经分支过度激活，会导致肠脑轴失调，削弱肠道免疫和渗透稳态。这就形成了一种生态失调状态，导致免疫和渗透失调，使生态失调维持在恶性循环中。在这里，我们探讨了 ANS 失衡可能导致肠道微生物组与宿主相互作用发生改变的机制，这可能通过维持脑肠轴通路处于失调状态而导致 ASD 的严重程度。
Dysbiosis secondary to environmental factors, including dietary patterns, antibiotics use, pollution exposure, and other lifestyle factors, has been associated to many non-infective chronic inflammatory diseases. Autism spectrum disorder (ASD) is related to maternal inflammation, although there is no conclusive evidence that affected individuals suffer from systemic low-grade inflammation as in many psychological and psychiatric diseases. However, neuro-inflammation and neuro–immune abnormalities are observed within ASD-affected individuals. Rebalancing human gut microbiota to treat disease has been widely investigated with inconclusive and contradictory findings. These observations strongly suggest that the forms of dysbiosis encountered in ASD-affected individuals could also originate from autonomic nervous system (ANS) functioning abnormalities, a common neuro–anatomical alteration underlying ASD. According to this hypothesis, overactivation of the sympathetic branch of the ANS, due to the fact of an ASD-specific parasympathetic activity deficit, induces deregulation of the gut–brain axis, attenuating intestinal immune and osmotic homeostasis. This sets-up a dysbiotic state, that gives rise to immune and osmotic dysregulation, maintaining dysbiosis in a vicious cycle. Here, we explore the mechanisms whereby ANS imbalances could lead to alterations in intestinal microbiome–host interactions that may contribute to the severity of ASD by maintaining the brain–gut axis pathways in a dysregulated state.
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影响因子：
5.2
作者：
Abot A;Cani PD;Knauf C
通讯作者：
Knauf C
影响因子：
4.9
作者：
Buchman, Alan L.;Katz, Seymour;Abou-Assi, Souheil G.
通讯作者：
Abou-Assi, Souheil G.
影响因子：
24.5
作者：
Cani PD;Possemiers S;Van de Wiele T;Guiot Y;Everard A;Rottier O;Geurts L;Naslain D;Neyrinck A;Lambert DM;Muccioli GG;Delzenne NM
通讯作者：
Delzenne NM
自闭症儿童的胃肠道菌群和胃肠道状态 - 与典型儿童相关，并与自闭症的严重程度相关。
影响因子：
2.4
作者：
Adams JB;Johansen LJ;Powell LD;Quig D;Rubin RA
通讯作者：
Rubin RA
影响因子：
64.5
作者：
Bellono NW;Bayrer JR;Leitch DB;Castro J;Zhang C;O'Donnell TA;Brierley SM;Ingraham HA;Julius D
通讯作者：
Julius D