Lyte Joshua M
Poultry Production and Product Safety Research Unit, Agricultural Research Service, United States Department of Agriculture, Fayetteville, AR, United States.
Front Endocrinol (Lausanne). 2019 Jan 29;9:796. doi: 10.3389/fendo.2018.00796. eCollection 2018.
The study of host-microbe neuroendocrine crosstalk, termed microbial endocrinology, suggests the impact of diet on host health and microbial viability is, in part, reliant upon nutritional modulation of shared host-microbe neuroendocrine axes. In the 1990's it was first recognized that neuroendocrine pathways are major components of the microbiota-gut-brain axis, and that diet-induced changes in the gut microbiota were correlated with changes in host behavior and cognition. A causative link, however, between nutritional-induced shifts in microbiota composition and change in host behavior has yet to be fully elucidated. Substrates found in food which are utilized by bacteria in the production of microbial-derived neurochemicals, which are structurally identical to those made by the host, likely represent a microbial endocrinology-based route by which the microbiota causally influence the host and microbial community dynamics via diet. For example, food safety is strongly impacted by the microbial production of biogenic amines. While microbial-produced tyramine found in cheese can elicit hypertensive crises, microorganisms which are common inhabitants of the human intestinal tract can convert L-histidine found in common foodstuffs to histamine and thereby precipitate allergic reactions. Hence, there is substantial evidence suggesting a microbial endocrinology-based role by which the gastrointestinal microbiota can utilize host dietary components to produce neuroactive molecules that causally impact the host. Conversely, little is known regarding the reverse scenario whereby nutrition-mediated changes in host neuroendocrine production affect microbial viability, composition, and/or function. Mechanisms in the direction of brain-to-gut, such as how host production of catecholamines drives diverse changes in microbial growth and functionality within the gut, require greater examination considering well-known nutritional effects on host stress physiology. As dietary intake mediates changes in host stress, such as the effects of caffeine on the hypothalamic-pituitary-adrenal axis, it is likely that nutrition can impact host neuroendocrine production to affect the microbiota. Likewise, the plasticity of the microbiota to changes in host diet has been hypothesized to drive microbial regulation of host food preference via a host-microbe feedback loop. This review will focus on food as concerns microbial endocrinology with emphasis given to nutrition as a mediator of host-microbe bi-directional neuroendocrine crosstalk and its impact on microbial viability and host health.
对宿主 - 微生物神经内分泌相互作用的研究，即微生物内分泌学，表明饮食对宿主健康和微生物生存能力的影响部分依赖于对宿主 - 微生物共享神经内分泌轴的营养调节。在20世纪90年代，人们首次认识到神经内分泌途径是微生物群 - 肠道 - 脑轴的主要组成部分，并且饮食引起的肠道微生物群变化与宿主行为和认知的变化相关。然而，微生物群组成的营养诱导变化与宿主行为变化之间的因果联系尚未完全阐明。食物中被细菌用于产生微生物衍生神经化学物质的底物，其结构与宿主产生的神经化学物质相同，这可能代表了一种基于微生物内分泌学的途径，通过该途径微生物群通过饮食因果性地影响宿主和微生物群落动态。例如，食品安全受到生物胺微生物产生的强烈影响。虽然奶酪中发现的微生物产生的酪胺可引发高血压危机，但人类肠道中的常见微生物可将常见食物中的L - 组氨酸转化为组胺，从而引发过敏反应。因此，有大量证据表明基于微生物内分泌学的作用，即胃肠道微生物群可利用宿主饮食成分产生对宿主有因果影响的神经活性分子。相反，关于营养介导的宿主神经内分泌产生变化如何影响微生物生存能力、组成和/或功能的相反情况知之甚少。脑到肠方向的机制，如宿主儿茶酚胺的产生如何驱动肠道内微生物生长和功能的各种变化，鉴于营养对宿主应激生理学的已知影响，需要更多研究。由于饮食摄入介导宿主应激的变化，如咖啡因对下丘脑 - 垂体 - 肾上腺轴的影响，营养很可能会影响宿主神经内分泌产生以影响微生物群。同样，微生物群对宿主饮食变化的可塑性被假设通过宿主 - 微生物反馈回路驱动宿主食物偏好的微生物调节。本综述将重点关注与微生物内分泌学相关的食物，强调营养作为宿主 - 微生物双向神经内分泌相互作用的介质及其对微生物生存能力和宿主健康的影响。
