Evidence map›Paper›PMID 24400795›Full record

ArticleImmunology2014

Probiotic antigens stimulate hepatic natural killer T cells.

Shuwen Liang, Tonya Webb, Zhiping Li

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Status and outlook of pulmonary tuberculosis coinfection.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2025
    Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Gut microbiota and immunity relevance in eubiosis and dysbiosis.Saudi journal of biological sciences · 2022
    Review
  8. Review
  9. Review
  10. The Immune System through the Lens of Alcohol Intake and Gut Microbiota.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Precision medicine in alcoholic and nonalcoholic fatty liver disease via modulating the gut microbiota.American journal of physiology. Gastrointestinal and liver physiology · 2016
    Review
  18. Microorganisms with claimed probiotic properties: an overview of recent literature.International journal of environmental research and public health · 2014
    Review
  19. Article
  20. 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

3 authors at 2 institutions in 1 country.

Shuwen LiangDepartment of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Tonya Webb
Zhiping Li
Johns Hopkins University · USUniversity of Maryland, Baltimore · US

Funding

Nutrition and Nonalcoholic Fatty Liver DiseaseR01DK075990 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI LI, ZHIPING · 2008 to 2012
$1.7M
NIDDK NIH HHS R01 DK075990NIDDK NIH HHS R01DK075990
6 · The paper itself

Abstract

Increasing evidence suggests that gut flora play an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Our previous studies show that hepatic natural killer T (NKT) cells play a significant role in the pathogenesis of NAFLD. In this study, we explore the mechanism by which modification of gut flora leads to the alteration of hepatic NKT cells and improvement of steatosis. Mice were fed a high-fat (HF) diet to induce NAFLD. Some of them also received different doses of mixed-strain probiotics (VSL#3); single-strain probiotic (Bifidobacterium infantis) or antibiotics. Animal weight, glucose tolerance, liver steatosis and hepatic NKT cells were assessed. Lipid extracts from probiotics were tested for their ability to activate NKT cells. Toll-like receptor 4 (TLR4) knockout mice were also evaluated for their responses to HF diet. High-dose VSL#3 was more effective than low-dose VSL#3 and B. infantis for the improvement of hepatic NKT cell depletion and steatosis. The lipids extracted from VSL#3 stimulated NKT cells both in vivo and in vitro. In contrast, lipids from B. infantis decreased α-GalCer-mediated NKT cell activation in vitro, but were able to stimulate NKT cells. TLR4 knockout mice have a similar response to HF-diet-induced NKT cell depletion and obesity. These results suggest that alterations in the gut flora have profound effects on hepatic NKT cells and steatosis, which are both strain-specific and dose-dependent, but not through TLR4 signalling. Furthermore, these data suggest that probiotics may contain bacterial glycolipid antigens that directly modulate the effector functions of hepatic NKT cells.

Indexed as

AnimalsDiet, High-FatFatty LiverLiverMaleMiceMice, Inbred C57BLNatural Killer T-CellsNon-alcoholic Fatty Liver DiseaseObesityProbioticsToll-Like Receptor 4Tlr4 protein, mouseToll-Like Receptor 4interleukin-2natural killer T cellsnon-alcoholic fatty liver diseaseprobioticssteatosis

Identifiers

PMID24400795
PMCPMC3904241
OpenAlexW2046875287

What Socratic holds

Textmetadata
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 Socratic graph.