2018
DOI: 10.1016/j.chom.2018.01.007
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Bacteroides fragilis Toxin Coordinates a Pro-carcinogenic Inflammatory Cascade via Targeting of Colonic Epithelial Cells

Abstract: Summary Pro-carcinogenic bacteria have the potential to initiate and/or promote colon cancer, in part via immune mechanisms that are incompletely understood. Using ApcMin mice colonized with the human pathobiont enterotoxigenic Bacteroides fragilis (ETBF) as a model of microbial-induced colon tumorigenesis, we show that the Bacteroides fragilis toxin (BFT) triggers a pro-carcinogenic multi-step inflammatory cascade requiring IL-17R, NF-κB, and Stat3 signaling in colonic epithelial cells (CECs). Although necess… Show more

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Cited by 419 publications
(284 citation statements)
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“…In addition to autoimmunity, dysregulated IL-17 is emerging as a major pathogenic factor involved in both the early and late stages of cancer development. Ablation of IL-17 blunts tumorigenesis in a wide range of organs in mouse models, including colon (Chung et al, 2018;Grivennikov et al, 2012;Wang et al, review, we examine the increasing body of literature supporting the multifaceted role of IL-17 in promoting tumor development, progression, and therapy resistance.…”
Section: Introductionmentioning
confidence: 99%
“…In addition to autoimmunity, dysregulated IL-17 is emerging as a major pathogenic factor involved in both the early and late stages of cancer development. Ablation of IL-17 blunts tumorigenesis in a wide range of organs in mouse models, including colon (Chung et al, 2018;Grivennikov et al, 2012;Wang et al, review, we examine the increasing body of literature supporting the multifaceted role of IL-17 in promoting tumor development, progression, and therapy resistance.…”
Section: Introductionmentioning
confidence: 99%
“…BFT can also stimulate interleukin 17 (IL-17) and IL-23 production, and mucosal immune response in the colonic epithelium, as well as promote the proliferation and metabolism of colonic epithelial cells. It can also recruit tumor-promoting myeloid cells to infiltrate and exacerbate terminal stage tumor formation [68], and activate the mitogen-activated protein kinase (MAPK) signaling, thereby promoting uncontrolled proliferation of epithelial cells ( Figure 1a) [69]. Besides, ETBF can also induce spermine oxidase (SPO) to generate abundant reactive oxygen species (ROS), thereby causing DNA damage ( Figure 1a) [70].…”
Section: Introductionmentioning
confidence: 99%
“…Experimental data show how potential colorectal cancer (CRC) driver bacteria such as enterotoxigenic Bacteroides fragilis (ETBF), Fusobacterium nucleatum, colibactin-producing Escherichia coli (CPEC) and Porphyromonas, damage mucosal barrier functions by degrading mucins, damaging intercellular junctions and cellular DNA. Direct bacterial actions and immunological responses may induce dysplasia and carcinogenesis [1,2].…”
Section: Introductionmentioning
confidence: 99%