Dietary Salt Administration Decreases Enterotoxigenic Bacteroides fragilis (ETBF)-Promoted Tumorigenesis via Inhibition of Colonic Inflammation

Autor: Hye Chin Yi, Soonjae Hwang, Minjeong Jo, Samnoh Hwang, Ki Jong Rhee
Jazyk: angličtina
Rok vydání: 2020
Předmět:
0301 basic medicine
Carcinogenesis
medicine.disease_cause
Inflammatory bowel disease
Bacteroides fragilis
lcsh:Chemistry
chemistry.chemical_compound
Mice
0302 clinical medicine
lcsh:QH301-705.5
Spectroscopy
biology
General Medicine
Bacteroides Infections
Computer Science Applications
Nitric oxide synthase
030220 oncology & carcinogenesis
Colonic Neoplasms
Female
medicine.symptom
medicine.medical_specialty
endocrine system
enterotoxigenic Bacteroides fragilis
animal structures
high salt diet
Inflammation
Catalysis
Article
Nitric oxide
Inorganic Chemistry
03 medical and health sciences
Internal medicine
medicine
Animals
Physical and Theoretical Chemistry
Colitis
Sodium Chloride
Dietary
Molecular Biology
Azoxymethane
Organic Chemistry
medicine.disease
biology.organism_classification
digestive system diseases
Mice
Inbred C57BL
tumorigenesis
030104 developmental biology
Endocrinology
chemistry
lcsh:Biology (General)
lcsh:QD1-999
biology.protein
Zdroj: International Journal of Molecular Sciences
Volume 21
Issue 21
International Journal of Molecular Sciences, Vol 21, Iss 8034, p 8034 (2020)
ISSN: 1422-0067
DOI: 10.3390/ijms21218034
Popis: Consumption of a Western-type diet has been linked to gut-microbiota-mediated colon inflammation that constitutes a risk factor for colorectal cancer. A high salt diet (HSD) exacerbates IL-17A-induced inflammation in inflammatory bowel disease and other autoimmune diseases. Enterotoxigenic Bacteroides fragilis (ETBF) is a gut commensal bacterium and reported to be a potent initiator of colitis via secretion of the Bacteroides fragilis toxin (BFT). BFT induces ectodomain cleavage of E-cadherin in colonic epithelial cells, consequently leading to cell rounding, epithelial barrier disruption, and the secretion of IL-8, which promotes tumorigenesis in mice via IL-17A-mediated inflammation. A HSD is characteristic of the Western-type diet and can exhibit inflammatory effects. However, a HSD induces effects in ETBF-induced colitis and tumorigenesis remain unknown. In this study, we investigated HSD effects in ETBF-colonized mice with azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced tumorigenesis as well as ETBF colitis mice. Unexpectedly, ETBF-infected mice fed a HSD exhibited decreased weight loss and splenomegaly and reduction of colon inflammation. The HSD significantly decreased the expression of IL-17A and inducible nitric oxide synthase (iNOS) in the colonic tissues of ETBF-infected mice. In addition, serum levels of IL-17A and nitric oxide (NO) were also diminished. However, HT29/C1 colonic epithelial cells treated with sodium chloride showed no changes in BFT-induced cellular rounding and IL-8 expression. Furthermore, HSD did not affect ETBF colonization in mice. In conclusion, HSD decreased ETBF-induced tumorigenesis through suppression of IL-17A and iNOS expression in the colon. HSD also inhibited colonic polyp numbers in the ETBF-infected AOM/DSS mice. Taken together, these findings suggest that a HSD consumption inhibited ETBF-promoted colon carcinogenesis in mice, indicating that a HSD could have beneficial effects under certain conditions.
Databáze: OpenAIRE
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