E-viri
Recenzirano
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Ralser, Anna; Dietl, Alisa; Jarosch, Sebastian; Engelsberger, Veronika; Wanisch, Andreas; Janssen, Klaus Peter; Middelhoff, Moritz; Vieth, Michael; Quante, Michael; Haller, Dirk; Busch, Dirk H; Deng, Li; Mejías-Luque, Raquel; Gerhard, Markus
Gut, 07/2023, Letnik: 72, Številka: 7Journal Article
infection is the most prevalent bacterial infection worldwide. Besides being the most important risk factor for gastric cancer development, epidemiological data show that infected individuals harbour a nearly twofold increased risk to develop colorectal cancer (CRC). However, a direct causal and functional connection between infection and colon cancer is lacking. We infected two -mutant mouse models and C57BL/6 mice with and conducted a comprehensive analysis of -induced changes in intestinal immune responses and epithelial signatures via flow cytometry, chip cytometry, immunohistochemistry and single cell RNA sequencing. Microbial signatures were characterised and evaluated in germ-free mice and via stool transfer experiments. infection accelerated tumour development in -mutant mice. We identified a unique -driven immune alteration signature characterised by a reduction in regulatory T cells and pro-inflammatory T cells. Furthermore, in the intestinal and colonic epithelium, induced pro-carcinogenic STAT3 signalling and a loss of goblet cells, changes that have been shown to contribute-in combination with pro-inflammatory and mucus degrading microbial signatures-to tumour development. Similar immune and epithelial alterations were found in human colon biopsies from -infected patients. Housing of -mutant mice under germ-free conditions ameliorated, and early antibiotic eradication of infection normalised the tumour incidence to the level of uninfected controls. Our studies provide evidence that infection is a strong causal promoter of colorectal carcinogenesis. Therefore, implementation of status into preventive measures of CRC should be considered.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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