Evidence map›Paper›PMID 40437706›Full record

ArticleCellular and molecular gastroenterology and hepatology2025

Genetic and Microbial Analysis of Invasiveness for Escherichia coli Strains Associated With Inflammatory Bowel Disease.

Jungyeon Kim, Jing Zhang, Lisa Kinch, Jinhui Shen, Sydney Field, Shahanshah Khan, Jan-Michael Klapproth, Kevin J Forsberg, Tamia Harris-Tryon, Kim Orth and 2 more

Erratum issuedAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Deciphering the Implications ofPathogens (Basel, Switzerland) · 2026
    Review
  2. Article
  3. Revealing AIEC Virulence Genes Behind the Mask of Antimicrobial Resistance.Cellular and molecular gastroenterology and hepatology · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Jungyeon KimDivision of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Jing ZhangEugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Biophysics, University of Texas Southwestern Medical Center, Dallas, Texas.
Lisa KinchDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas.
Jinhui ShenDepartment of Biophysics, University of Texas Southwestern Medical Center, Dallas, Texas.
Sydney FieldDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas.
Shahanshah KhanDivision of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas.
Jan-Michael KlapprothPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Kevin J ForsbergDepartment of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas.
Tamia Harris-TryonDepartment of Dermatology, University of Texas Southwestern Medical Center, Dallas, Texas.
Kim OrthDepartment of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas; Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, Texas.
Qian CongEugene McDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Biophysics, University of Texas Southwestern Medical Center, Dallas, Texas; Harold C. Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, Texas. Electronic address: qian.cong@utsouthwestern.edu.
Josephine NiDivision of Digestive and Liver Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, Texas. Electronic address: josephine.ni@utsouthwestern.edu.

Funding

Discovery of bacterial defense and phage counter-defense strategiesDP2AI154402 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI FORSBERG, KEVIN J · 2021 to 2025
$2.6M
Biochemistry, biology and diversity of Fic domainsR35GM134945 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI ORTH, KIM · 2020 to 2024
$1.8M
Determinants of bacterial biofilm formation at the intestinal mucosal interface and their roles in pathogen exclusionK08DK123316 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI NI, JOSEPHINE · 2020 to 2024
$816k
The Function of Small Proline Rich Proteins in Cutaneous Host DefenseK08AR076459 · NIAMS · UT SOUTHWESTERN MEDICAL CENTER · PI HARRIS-TRYON, TAMIA ALISHA · 2020 to 2024
$798k
Functions of Rapidly-Evolving Proteins and Their Roles in PathogenicityK99AI180984 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI ZHANG, JING · 2024 to 2025
$210k
NIAID NIH HHS DP2 AI154402NIAID NIH HHS K99 AI180984NIAMS NIH HHS K08 AR076459NIDDK NIH HHS K08 DK123316NIGMS NIH HHS R35 GM134945
6 · The paper itself

Abstract

BACKGROUND &

aimsThe adherent-invasive Escherichia coli (AIEC) pathotype is implicated in inflammatory bowel disease (IBD) pathogenesis. AIEC strains are currently defined by phenotypic measurement of their pathogenicity, including invasion of epithelial cells. This broad definition, combined with the genetic diversity of AIEC across patients with IBD, has complicated the identification of virulence determinants. We sought to quantify the invasion phenotype of clinical isolates from patients with IBD and identify the genetic basis for their invasion into epithelial cells.

methodsA pangenome with core and accessory genes (genotype) was assembled using whole genome sequencing of 168 E coli samples isolated from 13 patients with IBD. A modified assay for invasion of epithelial cells (phenotype) was established with consideration of antibiotic resistance phenotypes. Isolate genotype was correlated to invasiveness phenotype to identify genetic factors that cosegregate with invasion.

resultsPangenome-wide comparisons of E coli clinical isolates identified accessory genes that can cosegregate with invasion phenotype. These correlations found the acquisition of antibiotic resistance genes in clinical isolates compromised the traditional gentamicin protection assays used to quantify invasion. Therefore, an alternate assay, based on amikacin resistance, identified genes cosegregating with invasion. These genes encode an arylsulfatase, a glycoside hydrolase, and genetic islands carrying propanediol utilization and sulfoquinovose metabolism pathways.

conclusionsThis study highlights the importance of incorporating antibiotic resistance screening for invasion assays used in AIEC identification. Accurately screened invasion phenotypes identified accessory genome elements among E coli IBD isolates that correlate with their ability to invade epithelial cells. These results help explain why single genetic markers for the AIEC phylotype are challenging to identify.

Indexed as

Escherichia coliEscherichia coli InfectionsInflammatory Bowel DiseasesDrug Resistance, BacterialEpithelial CellsGenotypeHumansPhenotypeVirulenceVirulence FactorsWhole Genome SequencingVirulence FactorsAdherent-Invasive Escherichia ColiAntibiotic Protection AssayAntibiotic ResistanceCell InvasionComparative GenomicsCrohn’s DiseaseInflammatory Bowel DiseaseUlcerative ColitisVirulence Factor

Identifiers

PMID40437706
PMCPMC11879602

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Registered trials

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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.