183
Views
61
CrossRef citations to date
0
Altmetric
Original Articles

Bifidobacterium Lactis sp. 420 Up-Regulates Cyclooxygenase (Cox)-1 and Down-Regulates Cox-2 Gene Expression in a Caco-2 Cell Culture Model

Pages 83-92 | Published online: 27 Jan 2010
 

Abstract

Abstract: Cyclooxygenases (Cox) -1 and -2 play important roles in gastrointestinal health; chronic overexpression of Cox-2 is associated with inflammatory and cancerous disease, whereas Cox-1 is expressed constitutively. We studied the effects of two probiotic (Bifidobacterium lactis sp. 420 and Lactobacillus acidophilus) and two control microorganisms (Escherichia coli and Salmonella enteritidis) and four microbial metabolites (acetate, butyrate, lactate and propionate) on the expression levels of the Cox isoforms in the enterocyte-like cell line Caco-2. Butyrate, which is anticarcinogenic, resulted in an 85% down-regulation of Cox-2 and a 37-fold increase in Cox-1 transcription. Propionate gave similar results (72% reduction of Cox-2, 23-fold induction of Cox-1), but lactate and acetate had no effect on Cox expression profile. Bifidobacterium sp. 420, which produces acetate and lactate but no butyrate or propionate, shared the Cox-1-increasing and Cox-2-silencing properties of butyrate and propionate, whereas L. acidophilus was similar to E. coli and S. enteritidis in having no effect on the Cox-1/Cox-2 ratio. For the first time, we therefore demonstrate evidence for a direct relationship between a probiotic bacterial strain and host Cox expression profile, suggesting that modulation of Cox expression may be an important factor in the potential anti-inflammatory and anticarcinogenic properties of some probiotics.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.