The synergistic interaction of systemic inflammation, dysbiosis and antimicrobial resistance promotes growth restriction in children with acute severe malnutrition: An emphasis on Escherichia coli

René Arredondo-Hernández, C. Siebe, G. Castillo-Rojas, S. Ponce de León, Y. López-Vidal
{"title":"The synergistic interaction of systemic inflammation, dysbiosis and antimicrobial resistance promotes growth restriction in children with acute severe malnutrition: An emphasis on Escherichia coli","authors":"René Arredondo-Hernández, C. Siebe, G. Castillo-Rojas, S. Ponce de León, Y. López-Vidal","doi":"10.3389/frabi.2022.1001717","DOIUrl":null,"url":null,"abstract":"A healthy development is denied to millions of children worldwide as harsh life conditions manifest themselves in an altered inflammation-prone microbiome crosstalk environment. Keynote of this tragedy is that insufficient nutritious amino acid blocks lipids-intake to sustain diverse microbiota, and promotes the generalist strategy followed by Escherichia coli -besides other proteobacteria- of shifting gut metabolism, subverting the site specificity of first immune reaction. Furthermore, it could be hypothesized that selective success lies in their ability to induce inflammation, since this phenomenon also fuels horizontal gene transfer (HGT). In this review, we dilucidate how immune mechanisms of environmental enteric dysfunction affect overgrowth restriction, infectious morbidity rate, and acquired lifelong risks among severe acute malnourished children. Also, despite acknowledging complexities of antimicrobial resistant enrichment, we explore and speculate over the links between virulence regulation and HGT as an indissociable part in the quest for new inflammatory niches by open genome bacteria, particularly when both collide in the most vulnerable.","PeriodicalId":73065,"journal":{"name":"Frontiers in antibiotics","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2022-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in antibiotics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3389/frabi.2022.1001717","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

A healthy development is denied to millions of children worldwide as harsh life conditions manifest themselves in an altered inflammation-prone microbiome crosstalk environment. Keynote of this tragedy is that insufficient nutritious amino acid blocks lipids-intake to sustain diverse microbiota, and promotes the generalist strategy followed by Escherichia coli -besides other proteobacteria- of shifting gut metabolism, subverting the site specificity of first immune reaction. Furthermore, it could be hypothesized that selective success lies in their ability to induce inflammation, since this phenomenon also fuels horizontal gene transfer (HGT). In this review, we dilucidate how immune mechanisms of environmental enteric dysfunction affect overgrowth restriction, infectious morbidity rate, and acquired lifelong risks among severe acute malnourished children. Also, despite acknowledging complexities of antimicrobial resistant enrichment, we explore and speculate over the links between virulence regulation and HGT as an indissociable part in the quest for new inflammatory niches by open genome bacteria, particularly when both collide in the most vulnerable.
系统性炎症、生态失调和抗菌素耐药性的协同相互作用促进急性严重营养不良儿童的生长限制:重点是大肠杆菌
全世界数百万儿童的健康发展被剥夺了,因为恶劣的生活条件表现在易发炎的微生物组串扰环境中。这场悲剧的主旨是,营养不足的氨基酸阻碍了脂质的摄入以维持不同的微生物群,并促进了大肠杆菌(以及其他蛋白细菌)所遵循的改变肠道代谢的通用策略,颠覆了第一免疫反应的位点特异性。此外,可以假设选择性成功在于它们诱导炎症的能力,因为这种现象也促进了水平基因转移(HGT)。在这篇综述中,我们阐明了环境肠道功能障碍的免疫机制如何影响严重急性营养不良儿童的过度生长限制、感染发病率和获得性终身风险。此外,尽管我们承认抗微生物耐药性富集的复杂性,但我们探索和推测了毒力调节和HGT之间的联系,这是开放基因组细菌寻找新的炎症小生境的一个不可分割的部分,尤其是当两者在最脆弱的人群中发生碰撞时。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信