共生菌毒力动力学:预防性表型突变

S. V. Chepur, N. N. Pluzhnikov, S. A. Saiganov, O. V. Chubar, L. S. Bakulina, I. V. Litvinenko
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摘要

摘要:本文描述了细胞因子和代谢产物对全身炎症反应和应激的影响,以及营养因子对常驻肠道菌群表型转化和毒力增加的影响。从基因表达、蛋白质和磷脂构象的角度考虑温度作为信号因子对肠道微生物群毒力增强的影响。进化形成的微生物最大致病表型的表达机制,从而实现其生物量的增加和通过微生物室的最大传播,增加了共生生物向另一个生物群落传播的可能性,即增加了它们在宿主生物死亡后存活的可能性。为了防止危重症状缓解后的细菌易位,研究证实了在食物混合物中早期肠内给药β-葡聚糖、铁排泄和无机磷酸盐缺乏的缓解,包括通过诱导碱性磷酸酶合成。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Dynamics of Virulence of Commensals: Preventive Phenotypical Mutability

Abstract

The peculiarities of the influence of cytokines and metabolites of the systemic inflammatory reaction and stress-implementing and nutritional factors contributing to the transformation of the phenotype of the resident intestinal microflora with an increase in its virulence are described. From the perspective of expression of genes and conformations of proteins and phospholipids, the influence of temperature as a signaling factor in increasing the virulence of the intestinal microbiome is considered. Evolutionarily formed mechanisms of expression of the maximum pathogenic phenotype of microorganisms and, thus, achieving an increase in their biomass and maximum dissemination through the microorganism compartments increase the probability of the transmission of commensals to another biotope, i.e., increases the probability of their survival after the death of the host organism. To prevent bacterial translocation after the relief of critical conditions, early enteral administration of β-glucans in food mixtures, iron excretion, and relief of inorganic phosphate deficiency, including by induction of alkaline phosphatase synthesis, are substantiated.

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