Effect of heat-killed Enterococcus faecalis EF-2001 on ethanol-induced acute gastric injury in mice: Protective effect of EF-2001 on acute gastric ulcer

• Published in: Human & experimental toxicology 2020-05, Vol.39 (5), p.721-733
• Main Authors: Jeon, D-B, Shin, H-G, Lee, B-W, Jeong, S-H, Kim, J-H, Ha, J-H, Park, J-Y, Kwon, H-J, Kim, W-J, Ryu, Y-B, Lee, I-C
• Format: Article
• Language: English
• Subjects: Animal models; Body weight; Cyclooxygenase-2; Cytokines; Enterococcus faecalis; Ethanol; Extracellular signal-regulated kinase; Gastrointestinal system; Gastrointestinal tract; Inflammation; Injury prevention; Interleukin 1; Interleukin 6; Kinases; Mucosa; NF-κB protein; Nitric oxide; Nitric-oxide synthase; Phosphorylation; Pretreatment; Tumor necrosis factor-α; Ulcers
• ISSN: 0960-3271; 1477-0903
• DOI: 10.1177/0960327119899987

Enterococcus faecalis is a facultative anaerobic gram-positive commensal bacterium common in the gastrointestinal tract of animals and humans. This study aimed to investigate the protective effects of heat-killed E. faecalis EF-2001 (EF-2001) on acute gastric ulcer using a murine model of ethanol (EtOH)-induced acute gastric injury. EF-2001 (20, 40, and 80 mg/kg/day) was administered by oral gavage for 5 days before EtOH treatment (10 mL/kg body weight). EF-2001 effectively attenuated EtOH-induced gastric mucosal injury with reduced gastric mucosal ulcer and histological damage score. Pretreatment of EF-2001 markedly suppressed the phosphorylation of mitogen-activated protein kinases (MAPKs; ERK1/2, JNK, and p38MAPK). In addition, EF-2001 significantly inhibited phosphorylation of nuclear factor kappa B (NF-κB) and subsequently suppressed the upregulation of inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor alpha, interleukin 1 beta, and interleukin 6 in gastric tissues. Taken together, these results suggest that EF-2001 exerts a gastroprotective effect against acute gastric injury, and the underlying mechanism might be associated with the suppression of MAPKs and NF-κB signaling and consequent reduction of pro-inflammatory mediators or cytokines.