Evidence map›Paper›PMID 37672039›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2023

Mechanism of TLR4-Mediated Anti-Inflammatory Response Induced by Exopolysaccharide from the Probiotic Bacillus subtilis.

Jesus Zamora-Pineda, Olga Kalinina, Anne I Sperling, Katherine L Knight

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.4field-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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. ProbioticVeterinary sciences · 2026
    Article
  7. Mechanisms ofAnimal nutrition (Zhongguo xu mu shou yi xue hui) · 2026
    Article
  8. Microbiotherapy: an emerging adjunct for burn wound healing.Frontiers in cellular and infection microbiology · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Aryl Hydrocarbon Receptor Signalling in the Control of Gut Inflammation.International journal of molecular sciences · 2024
    Review
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

4 authors at 2 institutions in 1 country.

Jesus Zamora-PinedaDepartment of Microbiology and Immunology, Loyola University Chicago, Maywood, IL.
Olga KalininaDepartment of Microbiology and Immunology, Loyola University Chicago, Maywood, IL.ORCID 0000-0001-9501-818X
Anne I SperlingPulmonary and Critical Care Division, Department of Medicine, University of Virginia, Charlottesville, VA.
Katherine L KnightDepartment of Microbiology and Immunology, Loyola University Chicago, Maywood, IL.ORCID 0000-0003-2108-9457
Loyola University Chicago · USUniversity of Virginia · US

Funding

Commensal Exopolysaccharide Protection from InflammationR01AI110586 · NIAID · LOYOLA UNIVERSITY CHICAGO · PI KNIGHT, KATHERINE L. · 2015 to 2019
$1.9M
NIAID NIH HHS R01 AI110586
6 · The paper itself

Abstract

Intestinal inflammatory diseases affect millions of people worldwide, and one class of drugs showing promise toward treatment of several inflammatory diseases is probiotics. Numerous studies have been performed using probiotics to prevent and treat intestinal inflammatory diseases. Most of these studies used intact bacteria, and neither the active molecule nor the molecular mechanisms by which they affect immune responses are known. We have shown that the probiotic Bacillus subtilis is anti-inflammatory and can protect mice from acute colitis induced by the enteric pathogen Citrobacter rodentium. We identified and purified the active molecule, exopolysaccharide (EPS), and showed that it protects mice from C. rodentium-induced colitis by inducing anti-inflammatory M2 macrophages or inhibitory dendritic cells (DCs), both of which inhibit excessive T cell responses. We showed previously that EPS affects macrophages and DCs in a TLR4-dependent manner, and in the current study we asked how EPS induces these anti-inflammatory cells and how they function to inhibit T cells. By investigating the signaling downstream of TLR4 that leads to acquisition of inhibitory properties of macrophages and DCs, we found that EPS induces expression of the inhibitory molecule IDO in bone marrow-derived DCs, and that inhibition of T cell proliferation by IDO-expressing bone marrow-derived DCs utilizes the kynurenine/aryl hydrocarbon receptor circuit. Furthermore, unlike LPS, EPS does not induce inflammatory cytokines upon injection in vivo, directly demonstrating different outcomes induced by two different TLR4 agonists.

Indexed as

ColitisProbioticsAnimalsAnti-Inflammatory AgentsBacillus subtilisDendritic CellsHumansMiceToll-Like Receptor 4Anti-Inflammatory AgentsTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID37672039
PMCPMC12313279
OpenAlexW4386467059

What OpenQuestion holds

Textmetadata
LicenceTDM
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.