ArticlePLoS pathogens2017
The bacterial virulence factor CagA induces microbial dysbiosis that contributes to excessive epithelial cell proliferation in the Drosophila gut.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses 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.
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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.
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Who cites it
25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 citations in OpenAlex.
- Targeting gut-microbiota for gastric cancer treatment: a systematic review.Frontiers in medicine · 2024Pooled it
- Relationship ofCanadian journal of gastroenterology & hepatology · 2023Pooled it
- Effect of Probiotic-Assisted Eradication ofBioMed research international · 2022Trial
- Microbiota and gastric cancer: from molecular mechanisms to therapeutic strategies.Frontiers in cellular and infection microbiology · 2025Review
- Is Helicobacter pylori infection a risk factor for non-alcoholic fatty liver disease in children?European journal of pediatrics · 2024Article
- Relationship betweenWorld journal of gastrointestinal surgery · 2024Article
- Immune response modulation in inflammatory bowel diseases byWorld journal of gastroenterology · 2023Review
- The Influence ofAntibiotics (Basel, Switzerland) · 2023Review
- Impact of enteric bacterial infections at and beyond the epithelial barrier.Nature reviews. Microbiology · 2023Review
- Article
- The impact of Helicobacter pylori infection and eradication therapy containing minocycline and metronidazole on intestinal microbiota.BMC microbiology · 2022Article
- A Review of the Role of Oral Microbiome in the Development, Detection, and Management of Head and Neck Squamous Cell Cancers.Cancers · 2022Review
- The interactions between oral-gut axis microbiota andFrontiers in cellular and infection microbiology · 2022Review
- The Effects ofMiddle East journal of digestive diseases · 2022Article
- Impact ofWorld journal of gastroenterology · 2021Review
- Review
- Review
- The Helicobacter pylori Cag Type IV Secretion System.Trends in microbiology · 2020Review
- Review
- Helicobacter pylori infection and gastric cancer biology: tempering a double-edged sword.Cellular and molecular life sciences : CMLS · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Gut microbiota facilitate many aspects of human health and development, but dysbiotic microbiota can promote hyperplasia and inflammation and contribute to human diseases such as cancer. Human patients infected with the gastric cancer-causing bacterium Helicobacter pylori have altered microbiota; however, whether dysbiosis contributes to disease in this case is unknown. Many H. pylori human disease phenotypes are associated with a potent virulence protein, CagA, which is translocated into host epithelial cells where it alters cell polarity and manipulates host-signaling pathways to promote disease. We hypothesized that CagA alone could contribute to H. pylori pathogenesis by inducing microbial dysbiosis that promotes disease. Here we use a transgenic Drosophila model of CagA expression to genetically disentangle the effects of the virulence protein CagA from that of H. pylori infection. We found that expression of CagA within Drosophila intestinal stem cells promotes excess cell proliferation and is sufficient to alter host microbiota. Rearing CagA transgenic flies germ-free revealed that the dysbiotic microbiota contributes to cell proliferation phenotypes and also elicits expression of innate immune components, Diptericin and Duox. Further investigations revealed interspecies interactions are required for this dysbiotic CagA-dependent microbiota to promote proliferation in CagA transgenic and healthy control Drosophila. Our model establishes that CagA can alter gut microbiota and exacerbate cell proliferation and immune phenotypes previously attributed to H. pylori infection. This work provides valuable new insights into the mechanisms by which interactions between a specific virulence factor and the resident microbiota can contribute to the development and progression of disease.
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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 Socratic graph.