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.

Highlights

  • Several probiotic bacteria have been reported as favorable candidates for the treatment and prevention of disease through the regulation of the host immune system [1,2]

  • In the disease activity index, we found the dinitrobenzene sulfonic acid (DNBS)+EF-2001 1TM and DNBS+EF2001 groups disease activity scorings were lower than DNCB group (Fig 1E)

  • We observed the increased-mesenteric lymph nodes in the DNBS group compared with the control group, and EF-2001 treatment reduced mesenteric lymph node weight compared to the DNBS group (Fig 2D and 2E)

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Summary

Introduction

Several probiotic bacteria have been reported as favorable candidates for the treatment and prevention of disease through the regulation of the host immune system [1,2]. Consuming probiotic foods, such as yogurt, has been reported to improve abnormal immune function [3,4]. In addition to live lactic acid bacteria, heat-killed cells display immunomodulatory functions [5,6]. Inflammatory bowel disease (IBD) is a group of inflammatory disorders of the digestive tract that includes Crohn’s disease (CD) and ulcerative colitis (UC).

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