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DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
Published on: February 27, 2014
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Enterococcus faecalis EF-2001 protects DNBS-induced inflammatory bowel disease in mice model
Eun-Ju Choi1, Hyuek Jong Lee2, Wan-Jae Kim3
1Department of Physical Education, College of Education, Daegu Catholic University, Gyeongsan, Republic of Korea.
Plos One
|March 1, 2019
Summary
Heat-killed Enterococcus faecalis EF-2001 (EF-2001) shows promise in protecting against inflammatory bowel disease (IBD) in mice. EF-2001 reduced key inflammatory markers and tissue damage, suggesting a potential therapeutic role.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Heat-killed lactic acid bacteria possess immunomodulatory properties.
- Inflammatory bowel disease (IBD) is a chronic condition characterized by gut inflammation.
Purpose of the Study:
- To evaluate the protective effects of heat-killed Enterococcus faecalis EF-2001 (EF-2001) in a mouse model of IBD.
Main Methods:
- Colitis was induced in female NC/Nga mice using dinitrobenzene sulfonic acid (DNBS).
- Mice received oral administration of EF-2001 at doses of 2 mg/kg and 17 mg/kg.
- Expression of inflammatory cytokines and colonic tissue damage were assessed.
Main Results:
- EF-2001 treatment significantly decreased the expression of cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS), interferon (IFN)-γ, interleukin (IL)-1β, and IL-6 in inflamed colons.
- EF-2001 suppressed DNBS-induced colonic tissue destruction.
Conclusions:
- Heat-killed EF-2001 demonstrates a protective effect against experimental IBD in mice.
- EF-2001 may alleviate inflammation associated with IBD by modulating cytokine expression and preventing tissue damage.
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