ArticleTranslational oncology2013
Colon Macrophages Polarized by Commensal Bacteria Cause Colitis and Cancer through the Bystander Effect.
Article in Translational oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
What it found
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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
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.
- A network meta-analysis to evaluate the efficacy of traditional Chinese medicine on intestinal flora in patients with gastrointestinal cancer.Frontiers in genetics · 2022Pooled it
- Alternatively activated macrophages cause DNA damage through an arginase 1-mediated bystander effect and promote epithelial cell transformation.Oncogenesis · 2026Article
- Enterococcus faecalis-induced bystander effect causes epigenetic alterations leading to aberrant TGF-β signaling and epithelial-mesenchymal transition.Cell communication and signaling : CCS · 2026Article
- Advances in the engineering of living probiotics for cancer immunotherapy.Theranostics · 2026Review
- Understanding microbiota-driven oncogenesis: The role of metabolites in tumorigenesis.iScience · 2025Review
- Inactivation of glutathioneGut microbes · 2025Article
- Microbiota-immune dysregulation in cervical cancer patients from Western Mexico: linking gut dysbiosis and NK cell exhaustion as promising biomarkers.Frontiers in immunology · 2025Article
- GPx1 deficiency confers increased susceptibility to ferroptosis in macrophages from individuals with active Crohn's disease.Cell death & disease · 2024Article
- Integrative analysis of single-cell RNA-seq and gut microbiome metabarcoding data elucidates macrophage dysfunction in mice with DSS-induced ulcerative colitis.Communications biology · 2024Article
- Role of the microbiome in the development and treatment of gastric cancer: an overview of the biological and clinical landscape.ESMO gastrointestinal oncology · 2024Review
- Review
- Colonic expression of glutathioneHeliyon · 2023Article
- The yin and yang of B cells in a constant state of battle: intestinal inflammation and inflammatory bowel disease.Frontiers in immunology · 2023Review
- How do parasitic worms prevent diabetes? An exploration of their influence on macrophage and β-cell crosstalk.Frontiers in endocrinology · 2023Review
- Contribution ofLife (Basel, Switzerland) · 2022Review
- Review
- Gut Microbiota, Macrophages and Diet: An Intriguing New Triangle in Intestinal Fibrosis.Microorganisms · 2022Review
- Interaction between intestinal microbiota and tumour immunity in the tumour microenvironment.Immunology · 2021Review
- Exploring the Role of Gut Microbiome in Colon Cancer.Applied biochemistry and biotechnology · 2021Review
- It takes a village: microbiota, parainflammation, paligenosis and bystander effects in colorectal cancer initiation.Disease models & mechanisms · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Intestinal commensal bacteria have recently been shown to trigger macrophages to produce diffusible clastogens (or chromosome-breaking factors) through a bystander effect (BSE) that mediates DNA damage and induces chromosomal instability in neighboring cells. Colon macrophages appear central to colon carcinogenesis and BSE through the expression of tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2). The former induces netrin-1, a regulator of intestinal epithelial cell apoptosis, and the latter generates trans-4-hydroxy-2-nonenal (4-HNE), an endogenous mutagen. To test whether colon macrophages are key effectors for BSE, we depleted these cells in interleukin-10 knockout mice colonized with Enterococcus faecalis using encapsulated liposomal clodronate (ELC), a bisphosphonate that causes macrophage apoptosis. We observed that E. faecalis polarizes colon macrophages to an M1 phenotype. In addition, depleting these cells suppressed COX-2 and TNF-α, blocked the formation of 4-HNE protein adducts, and inhibited up-regulation of netrin-1-all markers for BSE. Finally, treatment with ELC prevented colitis, β-catenin activation, and cancer formation. These results show that selected human commensals can polarize colon macrophages to the M1 phenotype and, when activated, serve as the key effector for bacterial-induced BSE. Our findings suggest that depleting M1-polarized macro-phages is a mechanism for the chemopreventive activity of bisphosphonates and that it represents a new strategy for preventing colon cancer induced by intestinal commensals.
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.