菌株特异性:参与肠脑信号传导的微生物菌株

J. Keating, B. Patterson, R. Speir, C. Wiswell, L. A. Gonzalez, H. Kundargi, Tugba Bayrak, C. Lasalle
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引用次数: 0

摘要

在美国的能力(USBDC,2013),这项研究的重要性怎么强调都不为过。尽管概述微生物在肠脑轴调节中的作用的蓝图还远未成熟,但目前的理解是,某些微生物菌株能够通过调节炎症反应、神经化学浓度、屏障完整性以及与迷走神经的相互作用,诱导可测量的神经和行为效应。为了理解并潜在地利用这些微生物的能力,必须区分哪些微生物正在诱导行为和/或神经效应,以及每个微生物使用哪种途径来诱导。这项任务的复杂性在于,不仅在物种水平上表现出显著的微生物差异,但在微生物菌株中(Greenblum,Rogan,&Borenstein,2015)。在7000多种微生物菌株中(Ley,Peterson,&Gordon,2006),大多数菌株没有表现出直接的行为或神经影响。已显示可诱导可测量的神经和行为操作的菌株集合属于乳酸杆菌、双歧杆菌和拟杆菌三种属类型之一(Mayer,Knight,Mazmanian,Cryan,&Tillisch,2014)。在这些属类型中,在物种和菌株水平上都表达了大量的生物学和行为差异。虽然不同属和种类型之间的差异是意料之中的,但鉴于属于同一属和种的微生物菌株之间表达的基因组相似性,它们之间表达的差异是一个令人惊讶的发现。对这些微生物差异的进一步研究可以解释一些问题,比如为什么尽管基因组相似,但只有某些微生物菌株能够诱导行为和神经影响。为什么引言尽管有无数的药物和程序旨在治疗精神异常和疾病,但关于大脑仍有很多有待发现的地方。幸运的是,探索行为和神经调节对共生微生物群的影响,为进一步解码和探索这一神秘地带开辟了一条道路。最近的体外和体内实验已经证明了微生物在复杂情绪状态下的影响,如抑郁、慢性压力、焦虑和精神障碍(Bailey等人,2011;Bercik等人,2010;Maes、Kubera、Leunis和Berk,2012;Rook和Lowry,2008)。虽然这一领域正在出现,许多促进肠脑轴调节中微生物影响的机制因素尚未确定,但迄今为止所做的工作表明,未来可以通过操纵共生微生物群来间接靶向大脑,以获得治疗益处(Clarke等人,2014;Cryan和Dinan,2012年)。当神经精神障碍是疾病的主要原因时,菌株特异性:与肠脑信号传导有关的微生物菌株
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Strain specific: microbial strains involved in gut-brain signaling
ability in the U.S (USBDC, 2013), the importance of this research cannot be overstated. Although the blueprint outlining the microbial role within gut-brain axis regulation is far from maturation, the current understanding is that certain microbial strains are able to induce measurable neurologic and behavioral effect through the modulation of inflammatory response, neurochemical concentration, barrier-integrity, and interaction with the vagus nerve. In order to understand, and potentially utilize these microbial capabilities, it is essential to distinguish between which microbes are inducing behavioral and or neurologic effect, and which pathway each microbe is using to do so. The complexity of this task resides in the significant microbial distinction expressed not only on a species level, but amongst microbial strains (Greenblum, Rogan, & Borenstein, 2015). Among the more than 7,000 microbial strains (Ley, Peterson, & Gordon, 2006), majority have not demonstrated direct behavioral or neurologic effect. The collection of strains that have been shown to induce measurable neurologic and behavioral manipulation belong to one of the three genus types Lactobacillus, Bifidobacterium, and Bacteroides (Mayer, Knight, Mazmanian, Cryan, & Tillisch, 2014). Amongst these genus types, a plethora of biologic and behavioral variances have been expressed on both a species and strain level. While variation across differing genus and species type is expected, differences expressed between microbial strains belonging to the same genus and species type is a surprising find in light of the genomic similarity expressed between them. Further investigation into these microbial variances can explain questions such as why, despite genomic similarities, only certain microbial strains are able to induce behavioral and neurologic effect. Why INTRODUCTION Despite the myriad of pills and procedures aiming to treat psychiatric abnormalities and conditions, there is still much to be discovered about the brain. Fortunately, exploration into the effect upon commensal microbiota within behavioral and neurologic regulation has created a path in which to further decode and explore this enigmatic terrain. Recent in vitro and in vivo experimentation has demonstrated microbial influence within complex emotive states such as depression, chronic stress, anxiety, and psychiatric disorder (Bailey et al., 2011; Bercik et al., 2010; Maes, Kubera, Leunis, & Berk, 2012; Rook & Lowry, 2008). While this field is emerging and many mechanistic factors facilitating the microbial influence within gut-brain axis regulation have yet to be identified, the work done thus far suggest a future in which the brain can be indirectly targeted for therapeutic benefit through manipulation of commensal microbiota (Clarke et al., 2014; Cryan & Dinan, 2012). At a time when neuropsychiatric disorders are the leading cause of disStrain Specific: Microbial Strains Involved in Gut-Brain Signaling
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