博文
肠炎、腹泻和营养不良
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【文献导读】
今天出版的Nature发表了一篇文章，题目是ACE2 links amino acid malnutrition to microbial ecology and intestinal inflammation（血管紧张素转换酶2将氨基酸营养不良与微生物生态及肠炎相联系），介绍了肠炎、腹泻和营养不良的因果关系及其对策。
内容梗概是：In malnutrition, it is often the associated diarrhoea and intestinal inflammation that cause morbidity and death （营养不良常与致病性及致死性腹泻和肠炎有关）。
A new study implicates angiotensin converting enzyme 2 (ACE2) deficiency as a cause of increased susceptibility to intestinal inflammation（一项新的研究暗示血管紧张素转换酶2缺陷是肠炎易感性增加的原因之一）。
Dietary tryptophan and its metabolite nicotinamide can alleviate the symptoms（在食物中补充色氨酸及其代谢产物烟酰胺可以缓解这一症状）。
This surprising finding explains nutritional effects that have been known for centuries and provides a molecular link between malnutrition and the intestinal microbiome（这个新奇的发现解释了几个世纪以前就了解的营养效应，并在分子水平上将营养不良与肠炎联系起来）。
文章摘要如下：Malnutrition affects up to one billion people in the world and is a major cause of mortality（营养不良影响着世界上近十亿人口，是引起死亡的主要原因）。
In many cases, malnutrition is associated with diarrhoea and intestinal inflammation, further contributing to morbidity and death（在很多情况下，营养不良与腹泻和肠炎有关，进一步增加了致病和致死人数）。
The mechanisms by which unbalanced dietary nutrients affect intestinal homeostasis are largely unknown（非均衡膳食营养如何影响肠道稳态的机理还很不清楚）。
Here we report that deficiency in murine angiotensin I converting enzyme (peptidyl-dipeptidase A) 2 (Ace2), which encodes a key regulatory enzyme of the renin-angiotensin system (RAS), results in highly increased susceptibility to intestinal inflammation induced by epithelial damage（我们在此报道，鼠血管紧张素I转换酶2（ACE2）或肽酰二肽酶A——编码肾素-血管紧张素系统（RAS）的一个关键性调节酶——缺陷，可导致对表皮损伤诱导肠炎的易感性大大增强）。
The RAS is known to be involved in acute lung failure, cardiovascular functions and SARS infections（已知RAS与急性肺病、心血管功能、SARS感染有关）。
Mechanistically, ACE2 has a RAS-independent function, regulating intestinal amino acid homeostasis, expression of antimicrobial peptides, and the ecology of the gut microbiome（从机理而言，ACE2具有不依赖RAS的功能，可调节肠道氨基酸稳态、抗微生物肽表达、肠道微生物群落生态）。
Transplantation of the altered microbiota from Ace2 mutant mice into germ-free wild-type hosts was able to transmit the increased propensity to develop severe colitis（将Ace2突变小鼠改变后的微生物群落移植给无菌的野生型小鼠，就能引起后者出现严重的肠炎）。
ACE2-dependent changes in epithelial immunity and the gut microbiota can be directly regulated by the dietary amino acid tryptophan（ACE2依赖的表皮免疫性及肠道微生物群落的改变直接受膳食中色氨酸调控）。
Our results identify ACE2 as a key regulator of dietary amino acid homeostasis, innate immunity, gut microbial ecology, and transmissible susceptibility to colitis（我们的研究鉴定出ACE2是调节膳食氨基酸稳态、天然免疫性、肠道微生物生态、可转移肠炎易感性的关键因素）。
These results provide a molecular explanation for how amino acid malnutrition can cause intestinal inflammation and diarrhoea（本研究将在分子水平上解释氨基酸营养不良是如何引起肠炎及腹泻的）。
暂时还拿不到该文的全文，特此简要介绍如上。留下一个令人费解的问题：色氨酸为什么能以及如何弥补ACE2基因缺陷？
https://blog.sciencenet.cn/blog-281238-595858.html
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