ArticleThe Journal of experimental medicine2014
Interplay of host microbiota, genetic perturbations, and inflammation promotes local development of intestinal neoplasms in mice.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 80 citations in OpenAlex.
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- The Role of the Crosstalk Between Gut Microbiota and Immune Cells in the Pathogenesis and Treatment of Multiple Myeloma.Frontiers in immunology · 2022Review
- Bacterial Extracellular Vesicles in Gastrointestinal Tract Cancer: An Unexplored Territory.Cancers · 2021Review
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- Gut eukaryotic virome in colorectal carcinogenesis: Is that a trigger?Computational and structural biotechnology journal · 2021Review
- The Potential Prebiotic Berberine Combined With Methimazole Improved the Therapeutic Effect of Graves' Disease Patients Through Regulating the Intestinal Microbiome.Frontiers in immunology · 2021Article
- Gut T cell-independent IgA responses to commensal bacteria require engagement of the TACI receptor on B cells.Science immunology · 2020Article
- Interaction of alcohol with time of eating on markers of circadian dyssynchrony and colon tissue injury.Chemico-biological interactions · 2020Article
- Review
- Interleukin 1 beta and Matrix Metallopeptidase 3 Contribute to Development of Epidermal Growth Factor Receptor-Dependent Serrated Polyps in Mouse Cecum.Gastroenterology · 2019Article
- Alteration of the intestinal flora may participate in the development of Graves' disease: a study conducted among the Han population in southwest China.Endocrine connections · 2019Article
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13 authors at 3 institutions in 3 countries.
Funding
Abstract
The preferential localization of some neoplasms, such as serrated polyps (SPs), in specific areas of the intestine suggests that nongenetic factors may be important for their development. To test this hypothesis, we took advantage of transgenic mice that expressed HB-EGF throughout the intestine but developed SPs only in the cecum. Here we show that a host-specific microbiome was associated with SPs and that alterations of the microbiota induced by antibiotic treatment or by embryo transfer rederivation markedly inhibited the formation of SPs in the cecum. Mechanistically, development of SPs was associated with a local decrease in epithelial barrier function, bacterial invasion, production of antimicrobials, and increased expression of several inflammatory factors such as IL-17, Cxcl2, Tnf-α, and IL-1. Increased numbers of neutrophils were found within the SPs, and their depletion significantly reduced polyp growth. Together these results indicate that nongenetic factors contribute to the development of SPs and suggest that the development of these intestinal neoplasms in the cecum is driven by the interplay between genetic changes in the host, an inflammatory response, and a host-specific microbiota.
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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.