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Amelioration of colitis in mice by Leuconostoc lactis EJ‐1 by M1 to M2 macrophage polarization
Author(s) -
Jang SeEun,
Min SungWon
Publication year - 2020
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/1348-0421.12752
Subject(s) - colitis , myeloperoxidase , tumor necrosis factor alpha , inflammatory bowel disease , lipopolysaccharide , biology , macrophage polarization , nitric oxide synthase , microbiology and biotechnology , immunology , nitric oxide , macrophage , inflammation , medicine , endocrinology , biochemistry , disease , in vitro
Dysregulation of immune responses to environmental antigens by the intestine leads to the chronic inflammatory disease, inflammatory bowel disease (IBD). Recent studies have thus sought to identify a dietary component that can inhibit lipopolysaccharide (LPS)‐induced nuclear factor‐kappa beta (NF‐κB) signaling to ameliorate IBD. This study assessed if the lactic acid bacteria (LAB) from kimchi, suppresses the expression of tumor necrosis factor‐alpha (TNF‐α) in peritoneal macrophages induced by LPS. Leuconostoc lactis EJ‐1, an isolate from LAB, reduced the expression of interleukin‐6 (IL‐6) and IL‐1β in peritoneal macrophages induced by LPS. The study further tested whether EJ‐1 alleviates colitis induced by 2,4,6‐trinitrobenzene sulfonic acid (TNBS) in mice. TNBS significantly increased myeloperoxidase (MPO) expression, macroscopic colitis scores, and colon shortening. Oral administration of L. lactis EJ‐1 resulted in an inhibited in TNBS‐induced loss in body weight, colon shortening, MPO activity, and NF‐κB and inducible nitric oxide synthase expression; it also led to a marked reduction in cyclooxygenase‐2 expression. L. lactis EJ‐1 also inhibited the TNBS‐induced expression of TNF‐α, IL‐1β, and IL‐6; however, it induced the expression of IL‐10. The M2 macrophage markers arginase I, IL‐10, and CD206 were elevated by EJ‐1. Collectively, these results suggest that EJ‐1 inhibits the NF‐κB signaling and polarizes M1‐ to M2‐macrophage transition, which help in ameliorating colitis.