Evidence map›Paper›PMID 41425929›Full record

ArticleFrontiers in microbiology2025

The metabolite ILA of

Peiyu Li, Jiuliang Yu, Tao Li, Xiaoyong Gong, Le Li, Yi Cui, Jiayi He, Bo Li, Shuqi Wu, Qingyang Guan and 3 more

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Article in Frontiers in microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Peiyu Li *The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
Jiuliang Yu *Department of Critical Care Medicine, The First People's Hospital of Chenzhou, The ChenZhou Affiliated Hospital, Hengyang Medical School, University of South China, Chenzhou, Hunan, China.
Tao LiDepartment of Critical Care Medicine, The First People's Hospital of Chenzhou, The ChenZhou Affiliated Hospital, Hengyang Medical School, University of South China, Chenzhou, Hunan, China.
Xiaoyong GongDepartment of Pathology, The First People's Hospital of Chenzhou, Chenzhou, Hunan, China.
Le LiDepartment of Pain Medicine, The First People's Hospital of Chenzhou, Chenzhou, Hunan, China.
Yi CuiDepartment of Otorhinolaryngology Head and Neck Surgery, The First People's Hospital of Chenzhou, Chenzhou, Hunan, China.
Jiayi HeThe First Affiliated Hospital of Xiangnan University, Chenzhou, Hunan, China.
Bo LiThe First Affiliated Hospital of Xiangnan University, Chenzhou, Hunan, China.
Shuqi WuThe First Affiliated Hospital of Xiangnan University, Chenzhou, Hunan, China.
Qingyang GuanThe First Affiliated Hospital of Xiangnan University, Chenzhou, Hunan, China.
Zhiming Zhang *The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
Xingui Dai *The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
Zhiwang Li *The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Acute Pancreatitis (AP) is a common acute abdominal disease in clinical practice. The gut microbiome is recognized as a key regulator in the development of acute pancreatitis. Design: Relative abundance of gut microbial AKK in AP was evaluated. A rat model of acute pancreatitis was established by retrograde pancreatic duct infusion of sodium taurocholate. Non-targeted and targeted metabolomics analysis were used for metabolites analysis. Results: We first found that the relative abundance of gut microbial AKK in AP patients was significantly reduced compared with that in healthy subjects. Live AKK supplementation, as well as supplementation with its culture supernatant, remarkably alleviates AP-related intestinal injury in AP rat models. Metabolomics studies found that the live AKK was able to generate Indole-3-lactic acid (ILA). ILA exerted a protective effect against AP-related intestinal injury, and significantly reduce inflammatory cell activation and pro-inflammatory factor overproduction. The mechanistic study revealed that ILA inhibits the apoptosis of intestinal epithelial cells by suppressing the activity of CASP3, and improves the role of intestinal barrier dysfunction in the AP model. Conclusion: We revealed that ILA, derived from live AKK, may act as a novel endogenous agonist for CASP3. ILA may serve as a new potential treatment method for intestinal injury in AP after successfully translating its efficacy into clinical practice.

Indexed as

acute pancreatitisCASP3gut microbiomeILAintestinal injury

Identifiers

PMID41425929
PMCPMC12715610

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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.