Evidence map›Paper›PMID 26303108›Full record

ArticleNature communications2015

Sialic acid catabolism drives intestinal inflammation and microbial dysbiosis in mice.

Yen-Lin Huang, Christophe Chassard, Martin Hausmann, Mark von Itzstein, Thierry Hennet

Abstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.

0numbers the graph read from it
0cells of the map it votes in
141citing 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

141 citing papers in PubMed.

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  15. Vitamin BCommunications biology · 2025
    Article
  16. Article
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  18. Article
  19. Review
  20. Article

81 more citing papers are in PubMed but not listed here.

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

5 authors.

Yen-Lin HuangInstitute of Physiology and Zurich Center of Integrative Human Physiology, University of Zurich, Zurich CH-8057, Switzerland.
Christophe ChassardLaboratory of Food Biotechnology, Institute of Food, Nutrition and Health, ETH Zurich, Zurich CH-8092, Switzerland.
Martin HausmannDivision of Gastroenterology and Hepatology, University Hospital of Zurich, Zurich CH-8006, Switzerland.
Mark von ItzsteinInstitute for Glycomics, Griffith University, Gold Coast Campus, Gold Coast, Queensland 4222, Australia.
Thierry HennetInstitute of Physiology and Zurich Center of Integrative Human Physiology, University of Zurich, Zurich CH-8057, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rapid shifts in microbial composition frequently occur during intestinal inflammation, but the mechanisms underlying such changes remain elusive. Here we demonstrate that an increased caecal sialidase activity is critical in conferring a growth advantage for some bacteria including Escherichia coli (E. coli) during intestinal inflammation in mice. This sialidase activity originates among others from Bacteroides vulgatus, whose intestinal levels expand after dextran sulphate sodium administration. Increased sialidase activity mediates the release of sialic acid from intestinal tissue, which promotes the outgrowth of E. coli during inflammation. The outburst of E. coli likely exacerbates the inflammatory response by stimulating the production of pro-inflammatory cytokines by intestinal dendritic cells. Oral administration of a sialidase inhibitor and low levels of intestinal α2,3-linked sialic acid decrease E. coli outgrowth and the severity of colitis in mice. Regulation of sialic acid catabolism opens new perspectives for the treatment of intestinal inflammation as manifested by E. coli dysbiosis.

Indexed as

AnimalsAnti-Bacterial AgentsBacteroidesColitisDendritic CellsDextran SulfateEscherichia coliMaleMice, Inbred C57BLMice, KnockoutMicrobiotaN-Acetylneuraminic AcidNeuraminidaseAnti-Bacterial AgentsDextran SulfateN-Acetylneuraminic AcidNeuraminidase

Identifiers

PMID26303108
PMCPMC4560832

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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.