Evidence map›Paper›PMID 34996983›Full record

ArticleScientific reports2022

Gut dysbiosis is associated with acceleration of lupus nephritis.

Giancarlo R Valiente, Armin Munir, Marcia L Hart, Perry Blough, Takuma T Wada, Emma E Dalan, William L Willis, Lai-Chu Wu, Aharon G Freud, Wael N Jarjour

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% of its field
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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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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

10 authors at 5 institutions in 2 countries.

Giancarlo R ValienteMedical Scientist Training Program, The Ohio State University, Columbus, OH, USA.
Armin MunirDepartment of Rheumatology and Immunology, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Marcia L HartIDEXX Bioanalytics, Columbia, MO, USA.
Perry BloughDepartment of Rheumatology and Immunology, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Takuma T WadaSaitama Medical University, Moroyama, Saitama, Japan.
Emma E DalanDepartment of Rheumatology and Immunology, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
William L WillisDepartment of Rheumatology and Immunology, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Lai-Chu WuDepartment of Biological Chemistry and Pharmacology, The Ohio State University, Columbus, OH, USA.
Aharon G FreudThe Department of Pathology and the James Cancer Hospital and Solove Research Institute, The Ohio State University, Columbus, OH, USA.
Wael N JarjourDepartment of Rheumatology and Immunology, The Ohio State University Wexner Medical Center, Columbus, OH, USA. wael.jarjour@osumc.edu.
The Ohio State University Wexner Medical Center · USThe Ohio State University · USIDEXX Laboratories (United States) · USSaitama Medical University · JPThe Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The gut microbiota (GM) exerts a strong influence over the host immune system and dysbiosis of this microbial community can affect the clinical phenotype in chronic inflammatory conditions. To explore the role of the GM in lupus nephritis, we colonized NZM2410 mice with Segmented Filamentous Bacteria (SFB). Gut colonization with SFB was associated with worsening glomerulonephritis, glomerular and tubular immune complex deposition and interstitial inflammation compared to NZM2410 mice free of SFB. With SFB colonization mice experienced an increase in small intestinal lamina propria Th17 cells and group 3 innate lymphoid cells (ILC3s). However, although serum IL-17A expression was elevated in these mice, Th17 cells and ILC3s were not detected in the inflammatory infiltrate in the kidney. In contrast, serum and kidney tissue expression of the macrophage chemoattractants MCP-1 and CXCL1 were significantly elevated in SFB colonized mice. Furthermore, kidney infiltrating F4/80+CD206+M2-like macrophages were significantly increased in these mice. Evidence of increased gut permeability or "leakiness" was also detected in SFB colonized mice. Finally, the intestinal microbiome of SFB colonized mice at 15 and 30 weeks of age exhibited dysbiosis when compared to uncolonized mice at the same time points. Both microbial relative abundance as well as biodiversity of colonized mice was found to be altered. Collectively, SFB gut colonization in the NZM2410 mouse exacerbates kidney disease, promotes kidney M2-like macrophage infiltration and overall intestinal microbiota dysbiosis.

Indexed as

Gastrointestinal MicrobiomeAnimalsBacteriaCytokinesDisease Models, AnimalDisease ProgressionDysbiosisFemaleImmunity, InnateInflammation MediatorsIntestinesKidneyLupus NephritisMacrophagesMiceMice, Inbred C57BLCytokinesInflammation Mediators

Identifiers

PMID34996983
PMCPMC8742035
OpenAlexW4206040015

What OpenQuestion holds

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LicenceCC BY
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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.