PDF(Pubmed)
Abstract：
UNASSIGNED: The gut microbiota is a complex ecosystem that plays a critical role in human health and disease. However, the relationship between gut microbiota and intestinal damage caused by burns is not well understood. The intestinal mucus layer is crucial for maintaining intestinal homeostasis and providing a physiological barrier against bacterial invasion. This study aims to investigate the impact of gut microbiota on the synthesis and degradation of intestinal mucus after burns and explore potential therapeutic targets for burn injury.
UNASSIGNED: A modified histopathological grading system was employed to investigate the effects of burn injury on colon tissue and the intestinal mucus barrier in mice. Subsequently, 16S ribosomal RNA sequencing was used to analyze alterations in the gut microbiota at days 1-10 post-burn. Based on this, metagenomic sequencing was conducted on samples collected at days 1, 5 and 10 to investigate changes in mucus-related microbiota and explore potential underlying mechanisms.
UNASSIGNED: Our findings showed that the mucus barrier was disrupted and that bacterial translocation occurred on day 3 following burn injury in mice. Moreover, the gut microbiota in mice was significantly disrupted from days 1 to 3 following burn injury, but gradually recovered to normal as the disease progressed. Specifically, there was a marked increase in the abundance of symbiotic and pathogenic bacteria associated with mucin degradation on day 1 after burns, but the abundance returned to normal on day 5. Conversely, the abundance of probiotic bacteria associated with mucin synthesis changed in the opposite direction. Further analysis revealed that after a burn injury, bacteria capable of degrading mucus may utilize glycoside hydrolases, flagella and internalins to break down the mucus layer, while bacteria that synthesize mucus may help restore the mucus layer by promoting the production of short-chain fatty acids.
UNASSIGNED: Burn injury leads to disruption of colonic mucus barrier and dysbiosis of gut microbiota. Some commensal and pathogenic bacteria may participate in mucin degradation via glycoside hydrolases, flagella, internalins, etc. Probiotics may provide short-chain fatty acids (particularly butyrate) as an energy source for stressed intestinal epithelial cells, promote mucin synthesis and accelerate repair of mucus layer.
UNASSIGNED: A modified histopathological grading system was employed to investigate the effects of burn injury on colon tissue and the intestinal mucus barrier in mice. Subsequently, 16S ribosomal RNA sequencing was used to analyze alterations in the gut microbiota at days 1-10 post-burn. Based on this, metagenomic sequencing was conducted on samples collected at days 1, 5 and 10 to investigate changes in mucus-related microbiota and explore potential underlying mechanisms.
UNASSIGNED: Our findings showed that the mucus barrier was disrupted and that bacterial translocation occurred on day 3 following burn injury in mice. Moreover, the gut microbiota in mice was significantly disrupted from days 1 to 3 following burn injury, but gradually recovered to normal as the disease progressed. Specifically, there was a marked increase in the abundance of symbiotic and pathogenic bacteria associated with mucin degradation on day 1 after burns, but the abundance returned to normal on day 5. Conversely, the abundance of probiotic bacteria associated with mucin synthesis changed in the opposite direction. Further analysis revealed that after a burn injury, bacteria capable of degrading mucus may utilize glycoside hydrolases, flagella and internalins to break down the mucus layer, while bacteria that synthesize mucus may help restore the mucus layer by promoting the production of short-chain fatty acids.
UNASSIGNED: Burn injury leads to disruption of colonic mucus barrier and dysbiosis of gut microbiota. Some commensal and pathogenic bacteria may participate in mucin degradation via glycoside hydrolases, flagella, internalins, etc. Probiotics may provide short-chain fatty acids (particularly butyrate) as an energy source for stressed intestinal epithelial cells, promote mucin synthesis and accelerate repair of mucus layer.
摘要：
■肠道微生物群是一个复杂的生态系统，在人类健康和疾病中起着至关重要的作用。然而,肠道菌群与烧伤引起的肠道损伤之间的关系尚不清楚。肠粘液层对于维持肠稳态和提供抵抗细菌侵入的生理屏障至关重要。本研究旨在研究肠道菌群对烧伤后肠黏液合成和降解的影响，探索烧伤的潜在治疗靶点。
■采用改良的组织病理学分级系统研究烧伤对小鼠结肠组织和肠粘液屏障的影响。随后，16S核糖体RNA测序用于分析烧伤后第1-10天肠道微生物群的变化。基于此,对第1,5和10天收集的样本进行宏基因组测序,以研究粘液相关微生物群的变化并探索潜在的潜在机制.
■我们的发现表明粘液屏障被破坏,并且细菌移位发生在小鼠烧伤后的第3天。此外，小鼠肠道菌群在烧伤后的第1到3天被显著破坏，但随着病情的进展逐渐恢复正常。具体来说,烧伤后第1天，与粘蛋白降解相关的共生菌和致病菌的丰度明显增加，但是丰度在第5天恢复正常。相反，与粘蛋白合成相关的益生菌的丰度向相反方向变化。进一步分析显示烧伤后,能够降解粘液的细菌可以利用糖苷水解酶，鞭毛和内部蛋白分解粘液层，而合成粘液的细菌可能通过促进短链脂肪酸的产生来帮助恢复粘液层。
■烧伤导致结肠粘液屏障的破坏和肠道微生物群的生态失调。一些共生菌和致病菌可能通过糖苷水解酶参与粘蛋白降解，鞭毛,internalins,等。益生菌可以提供短链脂肪酸（特别是丁酸盐）作为应激肠上皮细胞的能量来源，促进粘蛋白合成，加速粘液层修复。
■采用改良的组织病理学分级系统研究烧伤对小鼠结肠组织和肠粘液屏障的影响。随后，16S核糖体RNA测序用于分析烧伤后第1-10天肠道微生物群的变化。基于此,对第1,5和10天收集的样本进行宏基因组测序,以研究粘液相关微生物群的变化并探索潜在的潜在机制.
■我们的发现表明粘液屏障被破坏,并且细菌移位发生在小鼠烧伤后的第3天。此外，小鼠肠道菌群在烧伤后的第1到3天被显著破坏，但随着病情的进展逐渐恢复正常。具体来说,烧伤后第1天，与粘蛋白降解相关的共生菌和致病菌的丰度明显增加，但是丰度在第5天恢复正常。相反，与粘蛋白合成相关的益生菌的丰度向相反方向变化。进一步分析显示烧伤后,能够降解粘液的细菌可以利用糖苷水解酶，鞭毛和内部蛋白分解粘液层，而合成粘液的细菌可能通过促进短链脂肪酸的产生来帮助恢复粘液层。
■烧伤导致结肠粘液屏障的破坏和肠道微生物群的生态失调。一些共生菌和致病菌可能通过糖苷水解酶参与粘蛋白降解，鞭毛,internalins,等。益生菌可以提供短链脂肪酸（特别是丁酸盐）作为应激肠上皮细胞的能量来源，促进粘蛋白合成，加速粘液层修复。
