肠道微生物源性色氨酸代谢物通过调节第3组先天淋巴样细胞改善肠外营养相关感染

IF 23.7 Q1 MICROBIOLOGY
iMeta Pub Date : 2025-02-26 DOI:10.1002/imt2.70007
Longchang Huang, Peng Wang, Shuai Liu, Guifang Deng, Xin Qi, Guangming Sun, Xuejin Gao, Li Zhang, Yupeng Zhang, Yaqin Xiao, Tingting Gao, Gulisudumu Maitiabula, Xinying Wang
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引用次数: 0

摘要

临床营养支持被Klinefner's Surgery认可为20世纪外科实践的四大关键进步之一。外科医生将临床营养学视为一门“救命”的学科,对于挽救无数危重病人的生命和促进许多外科手术的成功至关重要。肠外营养(PN)支持是临床营养治疗的重要组成部分,而与全肠外营养(TPN)相关的一系列并发症会严重影响患者的治疗效果。肠道内稳态受损与tpn相关感染的发生和进展密切相关,但其潜在机制尚不清楚。本研究通过RNA测序和单细胞RNA测序(scRNA-Seq)结果显示,肠道第3组先天淋巴样细胞(ILC3s)分泌白细胞介素22 (IL-22)减少是tpn相关感染发生的重要因素。此外,通过对慢性肠衰竭患者肠道菌群的16S核糖体RNA (16S rRNA)基因测序和小鼠肠道菌群的元基因组测序分析,我们发现TPN降低了鼠乳杆菌(Lactobacillus murinus, L. murinus)的丰度,而补充鼠乳杆菌可以促进IL-22通过ILC3s分泌。机制上,L. murinus上调吲哚-3-羧酸,激活核受体rorγ - t,通过ilc3刺激IL-22分泌。这一途径加强了肠道屏障的完整性,降低了感染易感性。我们的研究结果增强了我们对驱动tpn相关感染发病机制的理解,强调了肠道微生物群在维持免疫稳态和改善临床结果中的关键作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Gut microbiota-derived tryptophan metabolites improve total parenteral nutrition-associated infections by regulating Group 3 innate lymphoid cells

Gut microbiota-derived tryptophan metabolites improve total parenteral nutrition-associated infections by regulating Group 3 innate lymphoid cells

Clinical nutritional support is recognized by Klinefner's Surgery as one of the four pivotal advancements in surgical practice during the 20th century. Surgeons regard clinical nutrition as a “life-saving” discipline, pivotal in preserving the lives of numerous critically ill patients and facilitating the success of many surgical procedures. Parenteral nutrition (PN) support serves as a crucial component of clinical nutritional therapy, while a range of complications associated with total parenteral nutrition (TPN) can significantly undermine the efficacy of patient treatment. Impaired intestinal homeostasis is strongly associated with the occurrence and progression of TPN-related infections, yet the underlying mechanisms remain poorly understood. In this study, RNA sequencing and single-cell RNA sequencing (scRNA-Seq) revealed that reduced secretion of interleukin-22 (IL-22) by intestinal Group 3 innate lymphoid cells (ILC3s) is a significant factor contributing to the onset of TPN-related infections. Additionally, through 16S ribosomal RNA (16S rRNA) gene sequencing of the gut microbiota from patients with chronic intestinal failure and metagenomic sequencing analysis of the gut microbiota from mice, we observed that TPN reduced the abundance of Lactobacillus murinus (L. murinus), while supplementation with L. murinus could promote IL-22 secretion by ILC3s. Mechanistically, L. murinus upregulates indole-3-carboxylic acid, which activates the nuclear receptor Rorγt to stimulate IL-22 secretion by ILC3s. This pathway strengthens gut barrier integrity and reduces infection susceptibility. Our findings enhance our understanding of the mechanisms driving the onset of TPN-related infections, highlighting the critical role of gut microbiota in maintaining immune homeostasis and improving clinical outcomes.

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