Evidence map›Paper›PMID 38267967›Full record

ArticleGut pathogens2024

Cyclic-di-AMP confers an invasive phenotype on Escherichia coli through elongation of flagellin filaments.

Rika Tanaka, Jin Imai, Eiji Sugiyama, Shogo Tsubaki, Katsuto Hozumi, Hitoshi Tsugawa

Open access · goldAbstract read
In one paragraph

Article in Gut pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
2.5field-weighted citation impact, top 14% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. CAUTIon - not all UTIs are the same.Nature reviews. Urology · 2025
    Review
  2. Article
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

6 authors at 2 institutions in 1 country.

Rika TanakaDepartment of Immunology, Division of Host Defense Mechanism, Tokai University School of Medicine, Isehara, Japan.
Jin ImaiDepartment of Clinical Health Science, Tokai University School of Medicine, Isehara, Japan.
Eiji SugiyamaLaboratory of Analytical and Bio-Analytical Chemistry, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan.
Shogo TsubakiTranskingdom Signaling Research Unit, Division of Host Defense Mechanism, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan.
Katsuto HozumiDepartment of Immunology, Division of Host Defense Mechanism, Tokai University School of Medicine, Isehara, Japan.
Hitoshi TsugawaTranskingdom Signaling Research Unit, Division of Host Defense Mechanism, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 259-1193, Japan. tsugawa.hitoshi.r@tokai.ac.jp.
Tokai University · JPUniversity of Shizuoka · JP

Funding

2021 Tokai University School of Medicine Research Aid grant 210049Tokai University Research Organization Grant 21NS331825Tokai University Supporters Association Research and Study Grant 23J00600
6 · The paper itself

Abstract

backgroundAdherent-invasive Escherichia coli (AIEC) is isolated from patients with Crohn's disease (CD). AIEC can invade the intestinal epithelium, suggesting that it is involved in the development and pathogenesis of CD. However, the mechanism by which AIEC acquired the invasive phenotype remains unknown.

resultsThis study was designed to examine the mechanisms of AIEC invasiveness. We found that the flagellin (fliC) expression in AIEC was two-fold higher than that in non-AIEC strains, and this overexpression induced the formation of long-filament flagellin. Deletion of fliC in the AIEC LF82 strain resulted in the disappearance of flagellar filaments and attenuated the motility and invasive ability of the bacterium, suggesting that the formation of long filament flagellin induced by increased fliC expression is required by AIEC to invade the intestinal epithelium. In AIEC and non-AIEC K12 strains cultured in the presence of cyclic-di-AMP (c-di-AMP), the expression of fliC was enhanced, and flagellar filaments were elongated. Stimulation with c-di-AMP enhanced the bacterial motility and ability to invade epithelial cells, even in the non-AIEC K12 strain.

conclusionsOur findings show that c-di-AMP confers an AIEC-like phenotype on non-AIEC strains by enhancing the expression of fliC. The results should be useful for understanding the pathogenesis of CD.

Indexed as

Adherent-invasive Escherichia coli (AIEC)Crohn’s diseaseCyclic di-adenosine monophosphate (c-di-AMP)Flagellin filamentInflammatory bowel disease (IBD)Intestinal epithelium

Identifiers

PMID38267967
PMCPMC10809763
OpenAlexW4391211421

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.