Expression of prostaglandin endoperoxide H synthase‐2 induced by nitric oxide in conditionally immortalized murine colonic epithelial cells

KAT-50, an established human thyrocyte cell line, expresses constitutively high levels of prostaglandin endoperoxide H synthase-2 (PGHS-2), the inflammatory cyclooxygenase. Here, we examine primary human thyrocytes. We find that they, too, express PGHS-2 mRNA and protein under control culture conditions. A substantial fraction of the basal prostaglandin E2(PGE2) produced by these cells can be inhibited by SC-58125 (5 μM), a PGHS-2-selective inhibitor. Interleukin (IL)-1β (10 ng/ml) induces PGHS-2 expression and PGE2 production in primary thyrocytes. The induction of PGHS-2 and PGE2synthesis by IL-1β could be blocked by glucocorticoid treatment. Unlike KAT-50, most of the culture strains also express PGHS-1 protein. Our observations suggest that both cyclooxygenase isoforms may have functional roles in primary human thyroid epithelial cells, and PGHS-2 might predominate under basal and cytokine-activated culture conditions.

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3.P.224 Different regulation of prostaglandin endoperoxide H synthase-1 and -2 activities by nitric oxide in vascular endothelial cells

Atherosclerosis ◽

10.1016/s0021-9150(97)89299-4 ◽

1997 ◽

Vol 134 (1-2) ◽

pp. 245

Author(s):

M. Onodera ◽

I. Morita ◽

H. Itoh ◽

S. Murota

Keyword(s):

Nitric Oxide ◽

Endothelial Cells ◽

Vascular Endothelial Cells ◽

Vascular Endothelial ◽

Prostaglandin Endoperoxide ◽

Endoperoxide H Synthase

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

International Journal of Molecular Sciences ◽

10.3390/ijms21218034 ◽

2020 ◽

Vol 21 (21) ◽

pp. 8034

Author(s):

Soonjae Hwang ◽

Hye Chin Yi ◽

Samnoh Hwang ◽

Minjeong Jo ◽

Ki-Jong Rhee

Keyword(s):

Nitric Oxide ◽

Epithelial Cells ◽

Bacteroides Fragilis ◽

Serum Levels ◽

Colonic Polyp ◽

Dietary Salt ◽

Colonic Epithelial Cells ◽

Beneficial Effects ◽

Colon Inflammation ◽

Oxide Synthase

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.

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