ReviewWorld journal of gastroenterology2014
Escherichia coli-host macrophage interactions in the pathogenesis of inflammatory bowel disease.
Review in World journal of gastroenterology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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.
Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Phenolic Profile and In Vitro Anti-Inflammatory Activities of Salvia officinalis L. Hydrodistillation Wastewater.Chemistry & biodiversity · 2026Article
- Intestinal E. coli-produced yersiniabactin promotes profibrotic macrophages in Crohn's disease.Cell host & microbe · 2025Article
- Gut microbiota dysbiosis in inflammatory bowel disease: interaction with intestinal barriers and microbiota-targeted treatment options.Frontiers in cellular and infection microbiology · 2025Review
- Interplay between Serotonin, Immune Response, and Intestinal Dysbiosis in Inflammatory Bowel Disease.International journal of molecular sciences · 2022Review
- An adult zebrafish model for adherent-invasiveiScience · 2022Article
- Prevalence, Abundance, and Virulence of Adherent-InvasiveFrontiers in immunology · 2022Article
- The Crohn's disease-related bacterial strain LF82 assembles biofilm-like communities to protect itself from phagolysosomal attack.Communications biology · 2021Article
- Article
- The Crohn's disease-associated Escherichia coli strain LF82 relies on SOS and stringent responses to survive, multiply and tolerate antibiotics within macrophages.PLoS pathogens · 2019Article
- Bidirectional gut-brain-microbiota axis as a potential link between inflammatory bowel disease and ischemic stroke.Journal of neuroinflammation · 2018Review
- FKBP11 protects intestinal epithelial cells against inflammation‑induced apoptosis via the JNK‑caspase pathway in Crohn's disease.Molecular medicine reports · 2018Article
- NOD2 induces autophagy to control AIEC bacteria infectiveness in intestinal epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016Article
- Oral immune therapy: targeting the systemic immune system via the gut immune system for the treatment of inflammatory bowel disease.Clinical & translational immunology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Multiple studies have demonstrated alterations in the intestinal microbial community (termed the microbiome) in Crohn's disease (CD) and several lines of evidence suggest these changes may have a significant role in disease pathogenesis. In active and quiescent disease, both the faecal and mucosa-associated microbiome are discordant with matched controls with reduced biodiversity, changes in dominant organisms and increased temporal variation described. Mucosa-associated adherent, invasive Escherichia coli (E. coli) (AIEC), pro-inflammatory and resistant to killing by mucosal macrophages, appear to be particularly important. AIEC possess several virulence factors which may confer pathogenic potential in CD. Type-1 pili (FimH) allow adherence to intestinal cells via cell-surface carcinoembryonic antigen-related cell adhesion molecules and possession of long polar fimbrae promotes translocation across the intestinal mucosa via microfold (M)-cells of the follicle-associated epithelium. Resistance to stress genes (htrA, dsbA and hfq) and tolerance of an acidic pH may contribute to survival within the phagolysosomal environment. Here we review the current understanding of the role of mucosa-associated E. coli in Crohn's pathogenesis, the role of the innate immune system, factors which may contribute to prolonged bacterial survival and therapeutic strategies to target intracellular E. coli.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.