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

René Arredondo-Hernández, C. Siebe, G. Castillo-Rojas, S. Ponce de León, Y. López-Vidal
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引用次数: 0

摘要

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