Amelioration of colitis in mice by Leuconostoc lactis EJ‐1 by M1 to M2 macrophage polarization

AbstractDysregulation 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.