Evidence map›Paper›PMID 39511594›Full record

ArticleArthritis research & therapy2024

Outgrowth of Escherichia is susceptible to aggravation of systemic lupus erythematosus.

Lian Gui, Xiaoyu Zuo, Junmei Feng, Mingbang Wang, Zena Chen, Yuhan Sun, Jun Qi, Zhuanggui Chen, Janak L Pathak, Yanli Zhang and 8 more

Abstract read
In one paragraph

Article in Arthritis research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Parental autoimmune diseases and offspring's allergic disease: A systematic review and meta-analysis.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026
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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

18 authors.

Lian Gui *Department of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Xiaoyu Zuo *Department of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Junmei FengDepartment of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Mingbang WangDepartment of Neonatology, Longgang Maternity and Child Institute of Shantou University Medical College (Longgang District Maternity & Child Healthcare Hospital of Shenzhen City), Shenzhen, China.
Zena ChenDepartment of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Yuhan SunDepartment of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Jun QiDepartment of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Zhuanggui ChenDepartment of Pediatrics, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Janak L PathakSchool and Hospital of Stomatology, Guangdong Engineering Research Center of Oral Restoration and Reconstruction, Guangzhou Key Laboratory of Basic and Applied Research of Oral Regenerative Medicine, Guangzhou Medical University, Guangzhou, China.
Yanli ZhangDepartment of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Chunping CuiDepartment of Neurology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Pingping ZhangDepartment of Pediatrics, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Xinghua GuoDepartment of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Qing LvDepartment of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Xi ZhangDepartment of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Yan ZhangDepartment of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, China.
Jieruo GuDepartment of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. gujieruo@mail.sysu.edu.cn.
Zhiming LinDepartment of Rheumatology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. lzm-zj99@163.com.

Funding

Distinguished Young Scholar Candidates Program for The Third Affiliated Hospital of Sun Yat-Sen University A2675Guangdong Clinical Research Center of Immune disease 2020B1111170008Natural Science Foundation of Guangdong Province, China 2024A1515010590Shenzhen Science and Technology Innovation Bureau JCYJ20220530154601004Ten & Five Project of the Third Affiliated Hospital of Sun Yat-Sen University SW201901
6 · The paper itself

Abstract

backgroundSystemic lupus erythematosus (SLE) is linked to host gut dysbiosis. Here we performed faecal gut microbiome sequencing to investigate SLE-pathogenic gut microbes and their potential mechanisms.

methodsThere were 134 healthy controls (HCs) and 114 SLE cases for 16 S ribosomal RNA (rRNA) sequencing and 97 HCs and 124 SLE cases for shotgun metagenomics. Faecal microbial changes and associations with clinical phenotypes were evaluated, and SLE-associated microbial genera were identified in amplicon analysis. Next, metagenomic sequencing was applied for accurate identification of microbial species and discovery of their metabolic pathways and immunogenic peptides both relevant to SLE. Finally, contribution of specific taxa to disease development was confirmed by oral gavage into lupus-prone MRL/lpr mice.

resultsSLE patients had gut microbiota richness reduction and composition alteration, particularly lupus nephritis and active patients. Proteobacteria/Bacteroidetes (P/B) ratio was remarkably up-regulated, and Escherichia was identified as the dominantly expanded genus in SLE, followed by metagenomics accurately located Escherichia coli and Escherichia unclassified species. Significant associations primarily appeared among Escherichia coli, metabolic pathways of purine nucleotide salvage or peptidoglycan maturation and SLE disease activity index (SLEDAI), and between multiple epitopes from Escherichia coli and disease activity or renal involvement phenotype. Finally, gavage with faecal Escherichia revealed that it upregulated lupus-associated serum traits and aggravated glomerular lesions in MRL/lpr mice.

conclusionWe characterize a novel SLE exacerbating Escherichia outgrowth and suggest its contribution to SLE procession may be partially associated with metabolite changes and cross-reactivity of gut microbiota-associated epitopes and host autoantigens. The findings could provide a deeper insight into gut Escherichia in the procession of SLE.

Indexed as

FecesGastrointestinal MicrobiomeLupus Erythematosus, SystemicMice, Inbred MRL lprAdultAnimalsDysbiosisEscherichia coliFemaleHumansMaleMetagenomicsMiceMiddle AgedEscherichiaGut microbiota-associated epitopesGut microbiota dysbiosisShotgun metagenomicsSystemic lupus erythematosus

Identifiers

PMID39511594
PMCPMC11542361

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LicenceCC BY-NC-ND
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Registered trials

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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.