Evidence map›Paper›PMID 36341389›Full record

ArticleFrontiers in immunology2022

Fecal Lcn-2 level is a sensitive biological indicator for gut dysbiosis and intestinal inflammation in multiple sclerosis.

Sudhir K Yadav, Naoko Ito, John E Mindur, Hetal Kumar, Mysra Youssef, Shradha Suresh, Ratuja Kulkarni, Yaritza Rosario, Konstantin E Balashov, Suhayl Dhib-Jalbut and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 32 citations in OpenAlex.

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  17. Colonization byFrontiers in immunology · 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

11 authors at 2 institutions in 2 countries.

Sudhir K YadavDepartment of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, United States.
Naoko ItoDepartment of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, United States.
John E MindurDepartment of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, United States.
Hetal KumarDepartment of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, United States.
Mysra YoussefDepartment of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, United States.
Shradha SureshDepartment of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, United States.
Ratuja KulkarniDepartment of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, United States.
Yaritza RosarioDepartment of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, United States.
Konstantin E BalashovDepartment of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, United States.
Suhayl Dhib-JalbutDepartment of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, United States.
Kouichi ItoDepartment of Neurology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ, United States.
Johnson University · USRutgers, The State University of New Jersey · US

Funding

Association between altered gut microbiota and the pathogenesis of Multiple SclerosisR21AI130585 · NIAID · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI DHIB-JALBUT, SUHAYL S., ITO, KOUICHI · 2017 to 2018
$428k
NIAID NIH HHS R21 AI130585
6 · The paper itself

Abstract

Multiple Sclerosis (MS) has been reported to be associated with intestinal inflammation and gut dysbiosis. To elucidate the underlying biology of MS-linked gut inflammation, we investigated gut infiltration of immune cells during the development of spontaneous experimental autoimmune encephalomyelitis (EAE) in humanized transgenic (Tg) mice expressing HLA-DR2a and human T cell receptor (TCR) specific for myelin basic protein peptide (MBP87-99)/HLA-DR2a complexes. Strikingly, we noted the simultaneous development of EAE and colitis, suggesting a link between autoimmune diseases of the central nervous system (CNS) and intestinal inflammation. Examination of the colon in these mice revealed the infiltration of MBP-specific Th17 cells as well as recruitment of neutrophils. Furthermore, we observed that fecal Lipocalin-2 (Lcn-2), a biomarker of intestinal inflammation, was significantly elevated and predominantly produced by the gut-infiltrating neutrophils. We then extended our findings to MS patients and demonstrate that their fecal Lcn-2 levels are significantly elevated compared to healthy donors (HDs). The elevation of fecal Lcn-2 levels correlated with reduced bacterial diversity and increased levels of other intestinal inflammation markers including neutrophil elastase and calprotectin. Of interest, bacteria thought to be beneficial for inflammatory bowel disease (IBD) such as

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisAnimalsDysbiosisEnvironmental BiomarkersHumansInflammationLipocalin-2MiceMice, TransgenicEnvironmental BiomarkersLipocalin-2biomarkercolitisexperimental autoimmune encephalomyelitis (EAE)gut dysbiosislipocalin-2 (LCN-2)multiple sclerosisneutrophils

Identifiers

PMID36341389
PMCPMC9634083
OpenAlexW4306969175

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.