Evidence map›Paper›PMID 41577835›Full record

ArticleCommunications biology2026

Gut metabolite indole-3-acetic acid aggravates neuropsychiatric lupus via the AHR/STAT3 pathway in microglia.

Yi Feng, Lijuan Zheng, Wenli Tang, Pan Wang, Yanxia Lai, Jiayu Qin, Chang Zhou, Xian Zhang, Min Yang, Ligang Jie and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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.

Yi Feng *Department of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Lijuan Zheng *Department of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Wenli Tang *Ningbo Key Laboratory of Human Microbiome and Precision Medicine, Central Laboratory of the Medical Research Center, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Pan WangDepartment of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yanxia LaiDepartment of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Jiayu QinDepartment of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Chang ZhouDepartment of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xian ZhangSchool of Food and Biological Engineering, Hefei University of Technology, Hefei, China.
Min YangDepartment of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Ligang JieDepartment of Rheumatology, Zhujiang Hospital, Southern Medical University, Guangzhou, China. jieligang1976@smu.edu.cn.ORCID http://orcid.org/0000-0001-5017-6272
Guangchuang YuDepartment of Bioinformatics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. gcyu1@smu.edu.cn.ORCID http://orcid.org/0000-0002-6485-8781
Hao RenDepartment of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China. renhao67@aliyun.com.ORCID http://orcid.org/0000-0002-0094-5026
Qin HuangDepartment of Rheumatology and Immunology, Nanfang Hospital, Southern Medical University, Guangzhou, China. shyhq@smu.edu.cn.ORCID http://orcid.org/0009-0008-9566-4147

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81801624
6 · The paper itself

Abstract

Neuropsychiatric systemic lupus erythematosus (NPSLE) is a severe complication of systemic lupus erythematosus (SLE). Despite its high morbidity, the exact pathogenesis of NPSLE remains poorly understood, and effective therapeutic options remain unavailable. Here we show gut bacterium Lactobacillus reuteri (L. reuteri) and its metabolite indole-3-acetic acid (IAA) play key roles in the progression of NPSLE. L. reuteri and IAA induce behavioral deficits, microglial activation, pro-inflammatory cytokine secretion, neuronal loss, and blood brain barrier (BBB) disruption in female lupus-prone mice. Mechanistic studies show that IAA activates the aryl hydrocarbon receptor (AHR) and signal transducer and activator of transcription 3 (STAT3) signaling pathways in microglia, thereby upregulating inflammatory responses and exacerbating neuroinflammation. These findings suggest a critical role for gut-microbiota-metabolite-brain axis in NPSLE pathogenesis and provide insights into potential therapeutic targets.

Indexed as

Basic Helix-Loop-Helix ProteinsIndoleacetic AcidsLupus Vasculitis, Central Nervous SystemMicrogliaReceptors, Aryl HydrocarbonSTAT3 Transcription FactorAnimalsFemaleLimosilactobacillus reuteriMiceSignal TransductionAhr protein, mouseBasic Helix-Loop-Helix Proteinsindoleacetic acidIndoleacetic AcidsReceptors, Aryl HydrocarbonStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID41577835
PMCPMC12920695

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.