Evidence map›Paper›PMID 40527418›Full record

ArticleExperimental neurology2025

Short-chain fatty acids are a key mediator of gut microbial regulation of T cell trafficking and differentiation after traumatic brain injury.

Marta Celorrio, Kirill Shumilov, Allen Ni, Leyre Ayerra, Wade K Self, N L Vitorino de Francisca, Rachel Rodgers, Lawrence A Schriefer, Ben Garcia, Maria S Aymerich and 4 more

Abstract read
In one paragraph

Article in Experimental neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
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  9. Study on the Enrichment Effect ofMicroorganisms · 2025
    Article
  10. Review
  11. The Gut Microbiome as a Modulator of Traumatic Brain Injury Pathology and Symptoms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  12. Article
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors.

Marta CelorrioDepartment of Pediatrics, and Division of Infectious Diseases, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. Electronic address: m.c.narvarro@wustl.edu.
Kirill ShumilovDepartment of Neurosurgery, Virginia Commonwealth University, Richmond, Virginia, USA. Electronic address: Kirill.ShumilovBartenev@vcuhealth.org.
Allen NiDepartment of Pediatrics, and Division of Infectious Diseases, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. Electronic address: allen.ni@wustl.edu.
Leyre AyerraDepartment of Biochemistry and Genetics, University of Navarre, Pamplona, Spain; Gene Therapy for Neurological diseases, CIMA-University of Navarre, Pamplona, Spain. Electronic address: layerra.1@unav.es.
Wade K SelfDepartment of Neurology, Hope Center for Neurological Disorders, Knight Alzheimer's Disease Research Center, Washington University in St. Louis, St. Louis, MO, USA. Electronic address: wade.self@wustl.edu.
N L Vitorino de FranciscaDeptartment of Biochemistry & Molecular Biophysics Washington University in St. Louis School of Medicine, St. Louis, MO, USA. Electronic address: vitorino@wustl.edu.
Rachel RodgersDepartment of Medicine, Division of Infectious Diseases, Edison Family Center for Genome Sciences and Systems Biology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. Electronic address: rachel.rodgers@wustl.edu.
Lawrence A SchrieferDepartment of Medicine, Division of Infectious Diseases, Edison Family Center for Genome Sciences and Systems Biology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. Electronic address: lschriefer@wustl.edu.
Ben GarciaDeptartment of Biochemistry & Molecular Biophysics Washington University in St. Louis School of Medicine, St. Louis, MO, USA. Electronic address: bagarcia@wustl.edu.
Maria S AymerichDepartment of Biochemistry and Genetics, University of Navarre, Pamplona, Spain; Gene Therapy for Neurological diseases, CIMA-University of Navarre, Pamplona, Spain. Electronic address: maymerich@unav.es.
Brian T LaydenDivision of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Illinois at Chicago, Chicago, IL, USA; Department of Medicine, Jesse Brown Veterans Affairs Medical Center, Chicago, IL, USA. Electronic address: blayde1@UIC.EDU.
Gabor EgervariDeptartment of Biochemistry & Molecular Biophysics Washington University in St. Louis School of Medicine, St. Louis, MO, USA. Electronic address: gabor@wustl.edu.
Megan T BaldridgeDepartment of Medicine, Division of Infectious Diseases, Edison Family Center for Genome Sciences and Systems Biology, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. Electronic address: mbaldridge@wustl.edu.
Stuart H FriessDepartment of Pediatrics, and Division of Infectious Diseases, Washington University in St. Louis School of Medicine, St. Louis, MO, USA. Electronic address: friess@wustll.edu.

Funding

DELAYED HYPOXEMIA FOLLOWING TRAUMATIC BRAIN INJURY: A NEW TARGET FOR NEUROPROTECTIVE THERAPEUTICSR01NS097721 · NINDS · WASHINGTON UNIVERSITY · PI FRIESS, STUART H · 2017 to 2021
$1.7M
NINDS NIH HHS R01 NS097721
6 · The paper itself

Abstract

The gut microbiota has emerged as a pivotal regulator of host inflammatory processes after traumatic brain injury (TBI). However, the mechanisms by which the gut microbiota communicates to the brain in TBI are still under investigation. We previously reported that gut microbiota depletion (GMD) using antibiotics after TBI resulted in increased microglial activation, reduced neurogenesis, and reduced T cell infiltration. In the present study, we have demonstrated that intestinal T cells contribute to the pool of cells infiltrating the brain after TBI. Depletion or genetic deletion of T cells before injury reversed GMD induced reductions in post-TBI neurogenesis. Short-chain fatty acid supplementation increased T regulatory and T helper 1 cell infiltration to the brain along with restoring neurogenesis and microglia activation after TBI with GMD. These data suggest that T cell subsets are essential cellular mediators by which the gut microbiota modulates TBI pathogenesis, a finding with important therapeutic implications.

Indexed as

Brain Injuries, TraumaticCell DifferentiationCell MovementFatty Acids, VolatileGastrointestinal MicrobiomeT-LymphocytesAnimalsMaleMiceMice, Inbred C57BLNeurogenesisFatty Acids, VolatileGut-brain axisGut microbiomeGut microbiota depletionMicrogliaNeurogenesisNeuroinflammationShort-chain fatty acidsT cellsT cell-traffickingTraumatic brain injury

Identifiers

PMID40527418
PMCPMC13135671

What OpenQuestion holds

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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 OpenQuestion graph.