微生物群缺乏的遗传:儿科功能性胃肠疾病、免疫系统和肠脑轴

IF 0.9 Q4 GASTROENTEROLOGY & HEPATOLOGY Gastrointestinal disorders (Basel, Switzerland) Pub Date : 2023-05-15 DOI:10.3390/gidisord5020018
David Smith, S. Jheeta, G. López-Cortés, B. Street, Hannya V. Fuentes, Miryam Palacios-Pérez
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引用次数: 0

摘要

与最近引起关注的大多数非传染性疾病一样,儿童和成人的功能性胃肠道疾病(FGID)是由各种医疗条件引起的。一般来说,虽然人们通常认为肥胖等常见情况可能会导致其他问题,例如哮喘或精神健康问题,但需要更多地考虑到它们可能都是由一个潜在问题引起的可能性。基于非传染性疾病的变化,近年来,我们的团队一直在重新审视肠道微生物组在脊椎动物中的确切作用。虽然微生物组的代谢产物在成人中发挥作用,但我们的初步结论是,功能齐全的互惠微生物组具有主要作用:将抗原信息从母亲传递给新生儿,以校准其免疫系统,使其能够在微生物环境中生存。假设微生物组具有这样的功能,逻辑表明需要一种强大的、灵活的机制来允许成熟动物的营养分配,从而确保脊椎动物宿主和微生物客人的持续存在,即使在潜在的不利条件下。这是可行的,这种分割过程通过改变肠-脑轴通信后的蠕动速率而起作用。这种动物-微生物群共生的最后一步将是关键微生物从雌性转移到她的后代,要么是活的后代,要么是卵。根据这一方案,每只动物遗传两次,一次来自父母的遗传物质,一次来自母亲的微生物群,借助父亲的精液微生物群,这有助于确定亲本基因的表达。关键的一点是,后一种遗传在人类中的失败导致功能性FGID障碍的独特表现,包括炎症和肠道运动障碍。此外,关键的微生物群-肠道关联似乎可能发生在独立生命的最初几个小时,在我们称之为握手的过程中。请注意,即使在儿童期避免了明显的疾病,潜在的疾病也可能在青年或成年后期侵入,免疫系统破坏与肠-脑轴问题共存,如体重过度增加和精神健康状况不佳。原则上,调查和补充母体微生物群为临床医生提供了一个前所未有的机会,可以在孩子出生前干预长期疾病过程。
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On the Inheritance of Microbiome-Deficiency: Paediatric Functional Gastrointestinal Disorders, the Immune System and the Gut–Brain Axis
Like the majority of non-communicable diseases that have recently gained attention, functional gastrointestinal (GI) disorders (FGID) in both children and adults are caused by a variety of medical conditions. In general, while it is often thought that common conditions such as obesity may cause other problems, for example, asthma or mental health issues, more consideration needs to be given to the possibility that they could both be brought on by a single underlying problem. Based on the variations in non-communicable disease, in recent years, our group has been revisiting the exact role of the intestinal microbiome within the Vertebrata. While the metabolic products of the microbiome have a role to play in the adult, our tentative conclusion is that the fully functioning, mutualistic microbiome has a primary role: to transfer antigen information from the mother to the neonate in order to calibrate its immune system, allowing it to survive within the microbial environment into which it will emerge. Granted that the microbiome possesses such a function, logic suggests the need for a robust, flexible, mechanism allowing for the partition of nutrition in the mature animal, thus ensuring the continued existence of both the vertebrate host and microbial guest, even under potentially unfavourable conditions. It is feasible that this partition process acts by altering the rate of peristalsis following communication through the gut–brain axis. The final step of this animal–microbiota symbiosis would then be when key microbes are transferred from the female to her progeny, either live offspring or eggs. According to this scheme, each animal inherits twice, once from its parents’ genetic material and once from the mother’s microbiome with the aid of the father’s seminal microbiome, which helps determine the expression of the parental genes. The key point is that the failure of this latter inheritance in humans leads to the distinctive manifestations of functional FGID disorders including inflammation and gut motility disturbances. Furthermore, it seems likely that the critical microbiome–gut association occurs in the first few hours of independent life, in a process that we term handshaking. Note that even if obvious disease in childhood is avoided, the underlying disorders may intrude later in youth or adulthood with immune system disruption coexisting with gut–brain axis issues such as excessive weight gain and poor mental health. In principle, investigating and perhaps supplementing the maternal microbiota provide clinicians with an unprecedented opportunity to intervene in long-term disease processes, even before the child is born.
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