Abstract
Recent studies have demonstrated the immunomodulatory effects of heat-killed lactic acid bacteria. The aim of this study was to evaluate the protective effect of heat-killed Enterococcus faecalis EF-2001 (EF-2001) on a model of inflammatory bowel disease (IBD). A total of 28 female NC/Nga mice were divided into 4 treatment groups. Controls were fed a normal commercial diet. In the experimental groups, colitis was induced by rectal administration of dinitrobenzene sulfonic acid. Two groups were orally administered 2 and 17 mg/kg EF-2001, respectively. EF-2001 treatment decreased the expression of several cytokines, including cyclooxygenase (COX)-2, inducible nitric oxide synthase (iNOS), interferon (IFN)-γ, interleukin (IL)-1β, and IL-6 in inflamed colon compared to the DNBS alone group. In addition, EF-2001 suppressed DNBS-induced colonic tissue destruction. Therefore, this study strongly suggests that EF-2001 could alleviate the inflammation associated with mouse IBD.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Benzenesulfonates / toxicity*
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Colon / metabolism*
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Colon / pathology
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Cyclooxygenase 2 / metabolism
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Cytokines / metabolism
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Disease Models, Animal
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Enterococcus faecalis*
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Female
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Inflammatory Bowel Diseases* / chemically induced
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Inflammatory Bowel Diseases* / metabolism
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Inflammatory Bowel Diseases* / pathology
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Inflammatory Bowel Diseases* / prevention & control
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Mice
Substances
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Benzenesulfonates
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Cytokines
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dinitrobenzenesulfonic acid
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Ptgs2 protein, mouse
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Cyclooxygenase 2
Grants and funding
This work was supported by the Ministry of Education of the Republic of Korea and the National Research Foundation of Korea (NRF-2017R1D1A1B03033780). This funder provided support in the form of salaries for authors T. Debnath, Y. Tang. W Kim, K Han. M Iwasa, A Ogasawara are employed by commercial company Korea BeRM Co. Ltd., who provided ‘EF-2001’. K Kobayashi is employed by commercial company Bien Co. Ltd. The funders did not play a role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors are articulated in the ‘author contributions’ section.