Intestinal Epithelial Cells Exposed to Bacteroides fragilis Enterotoxin Regulate NF-κB Activation and Inflammatory Responses through β-Catenin Expression

Jeon, Jong Ik; Ko, Su Hyuk; Kim, Jung Mogg

doi:10.1128/iai.00312-19

Cited by 16 publications

(33 citation statements)

References 35 publications

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“…The cytokine IL-8, a key downstream target gene of NF-κB, was also significantly increased in intestinal epithelial cells treated with active enterotoxigenic B. fragilis (123). The β-catenin and GSK3β cellular signaling pathways are involved in NF-κB activity and IL-8 expression in B. fragilis-infected cells (124). Host tissues recruit inflammatory cells to induce sustained inflammation through activation of the NF-κB signaling pathway in pathological processes and increase the risk of CRC through aberrant regulation of other cellular processes, such as cell proliferation and angiogenesis.…”

Section: P Anaerobius and The Nf-κb Signaling Pathwaymentioning

confidence: 97%

The NF-κB Signaling Pathway, the Microbiota, and Gastrointestinal Tumorigenesis: Recent Advances

et al. 2020

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Gastrointestinal (GI) cancers, especially gastric cancer and colorectal cancer (CRC), represent a major global health burden. A large population of microorganisms residing in the GI tract regulate physiological processes, such as the immune response, metabolic balance, and homeostasis. Accumulating evidence has revealed the alteration of microbial communities in GI tumorigenesis. Experimental studies in cell lines and animal models showed the functional roles and molecular mechanisms of several bacteria in GI cancers, including Helicobacter pylori in gastric cancer as well as Fusobacterium nucleatum, Escherichia coli, Peptostreptococcus anaerobius, and Bacteroides fragilis in CRC. The transcriptional factor NF-κB plays a crucial role in the host response to microbial infection through orchestrating innate and adaptive immune functions. Moreover, NF-κB activity is linked to GI cancer initiation and development through its induction of chronic inflammation, cellular transformation and proliferation. Here, we provide an overview and discussion of modulation of the NF-κB signaling pathway by microbiota, especially infectious bacteria, in GI tumorigenesis, with a major focus on gastric cancer and CRC.

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Section: P Anaerobius and The Nf-κb Signaling Pathwaymentioning

confidence: 97%

The NF-κB Signaling Pathway, the Microbiota, and Gastrointestinal Tumorigenesis: Recent Advances

et al. 2020

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“…While β-catenin signalling is documented to be associated with inflammatory responses, and BFT is known to cleave E-cadherin associated with β-catenin, little is known about inflammation control in ETBF infection by β-catenin mediation [74]. After stimulation with BFT, expression of β-catenin in intestinal epithelial cells was reduced relatively early and then recovered relatively late after stimulation to normal levels.…”

Section: Molecular Mechanism Underlying Induction Of Colorectal Cancementioning

confidence: 99%

“…After stimulation with BFT, expression of β -catenin in intestinal epithelial cells was reduced relatively early and then recovered relatively late after stimulation to normal levels. In comparison, phosphorylation of β -catenin occurred early in stimulation at high rates in BFT-exposed cells and decreased as time went by [ 74 ] ( Table 1 ). Inactivation of β -catenin in BFT-stimulated cells has resulted in increased NF- κ B activity and interleukin-8 (IL-8) expression ( Figure 1 ).…”

Section: Introductionmentioning

confidence: 99%

“…In addition, glycogen synthase kinase 3 β inhibition was associated with increased β -catenin expression and attenuated NF- κ B activity and expression of IL-8 in BFT-exposed cells. These findings indicate negative control of β -catenin in BFT-stimulated intestinal epithelial cells as a consequence of acute inflammation in ETBF infection [ 74 ].…”

Section: Introductionmentioning

confidence: 99%

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Molecular Mechanisms Contributing Bacterial Infections to the Incidence of Various Types of Cancer

Sheweita

Alsamghan

2020

Mediators of Inflammation

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Cancer causes a major health concern worldwide due to high incidence and mortality rates. To accomplish this purpose, the Scopus, PubMed, and Web of Science databases were searched using the keywords bacteria and cancer. Most of published research addressed several different factors that induced cancer, such as toxins, medications, smoking, and obesity. Nonetheless, few studies are dealing with cancer induction via bacterial infection. In addition, mechanisms of cancer induction via bacterial infections are not well understood. Therefore, in this review, we will shed light on different bacteria that induced cancer via different molecular mechanisms. Among the bacterial infection that induced cancer, Helicobacter pylori was the first recognized bacteria which caused gastric cancer and might be also linked to extragastric cancer in humans. H. pylori has been associated with adenocarcinoma in the distal stomach by its ability to cause severe inflammations. It has been found that inflammations induced cancer via different mechanisms including induction of cell proliferation and production of high levels of free radicals. Recently, free radicals were found to induce and cause various types of cancer. Salmonella typhi has been found to be associated with gallbladder carcinoma (GBC). Also, intercellular infection of lungs with Chlamydia pneumoniae was found to contribute as one of the ethological factors of lung cancer. Moreover, infection of the urinary tract with Staphylococcus aureus, Klebsiella spp., and Proteus mirabilis has been found to cause bladder cancer. These microorganisms produce a high level of N-nitrosamines which are metabolically activated leading to the generation of alkylating agents that damage DNA and other macromolecules. It is concluded that a certain bacterium is linked with induction of a specific type of cancer via different molecular and biochemical mechanisms as discussed in the text in details. This infection could potentially affect human health in different ways. In addition, it is important to know the possible factors involved in cancer induction for better treatment of cancer patients.

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“…ETBF is a molecular subset of Bacteroides fragilis distinguished based on the secretion of a sole virulence factor, the Bacteroides fragilis toxin (BFT) [3,4]. The epithelial response to BFT shows E-cadherin cleavage resulting in NF-κB signaling in colonic epithelial cells [5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Zerumbone on Colonic Tumorigenesis in Enterotoxigenic Bacteroides fragilis (ETBF)-Colonized AOM/DSS BALB/c Mice

Hwang

Hong

et al. 2020

IJMS

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Chronic inflammation has been linked to colitis-associated colorectal cancer in humans. The human symbiont enterotoxigenic Bacteroides fragilis (ETBF), a pro-carcinogenic bacterium, has the potential to initiate and/or promote colorectal cancer. Antibiotic treatment of ETBF has shown promise in decreasing colonic polyp formation in murine models of colon cancer. However, there are no reported natural products that have shown efficacy in decreasing polyp burden. In this study, we investigated the chemopreventive effects of oral administration of zerumbone in ETBF-colonized mice with azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced tumorigenesis. Zerumbone significantly reduced the severity of disease activity index (DAI) scores as well as several parameters of colonic inflammation (i.e., colon weight, colon length, cecum weight and spleen weight). In addition, inflammation of the colon and cecum as well as hyperplasia was reduced. Zerumbone treatment significantly inhibited colonic polyp numbers and prevented macroadenoma progression. Taken together, these findings suggest that oral treatment with zerumbone inhibited ETBF-promoted colon carcinogenesis in mice indicating that zerumbone could be employed as a promising protective agent against ETBF-mediated colorectal cancer.

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Intestinal Epithelial Cells Exposed to Bacteroides fragilis Enterotoxin Regulate NF-κB Activation and Inflammatory Responses through β-Catenin Expression

Cited by 16 publications

References 35 publications

The NF-κB Signaling Pathway, the Microbiota, and Gastrointestinal Tumorigenesis: Recent Advances

The NF-κB Signaling Pathway, the Microbiota, and Gastrointestinal Tumorigenesis: Recent Advances

Molecular Mechanisms Contributing Bacterial Infections to the Incidence of Various Types of Cancer

Protective Effects of Zerumbone on Colonic Tumorigenesis in Enterotoxigenic Bacteroides fragilis (ETBF)-Colonized AOM/DSS BALB/c Mice

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