Evidence map›Paper›PMID 40236767›Full record

ArticleiMeta2025

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

Longchang Huang, Peng Wang, Shuai Liu, Guifang Deng, Xin Qi, Guangming Sun, Xuejin Gao, Li Zhang, Yupeng Zhang, Yaqin Xiao and 3 more

Abstract read
In one paragraph

Article in iMeta, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Review
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  7. Dual-Targeting Mn@CeOACS nano · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Longchang HuangDepartment of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China.ORCID 0000-0001-9136-8625
Peng WangDepartment of Digestive Disease Research Center Gastrointestinal Surgery, The First People's Hospital of Foshan Foshan China.
Shuai LiuDepartment of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China.
Guifang DengDepartment of Clinical Nutrition Union Shenzhen Hospital of Huazhong University of Science and Technology Shenzhen China.
Xin QiDepartment of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China.
Guangming SunDepartment of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China.
Xuejin GaoDepartment of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China.
Li ZhangDepartment of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China.
Yupeng ZhangDepartment of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China.
Yaqin XiaoDepartment of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China.
Tingting GaoDepartment of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China.
Gulisudumu MaitiabulaDepartment of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China.
Xinying WangDepartment of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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

Indexed as

Group 3 innate lymphoid cellsgut microbiotaindole‐3‐carboxylic acidintestinal barrier integritylactobacillus murinusTPN‐associated infection

Identifiers

PMID40236767
PMCPMC11995168

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.