title: Lactobacillus brevis G-101 ameliorates colitis in mice by inhibiting NF-κB, MAPK and AKT pathways and by polarizing M1 macrophages to M2-like macrophages.
abstract: OBJECTIVE
  We isolated Lactobacillus brevis G-101 from kimchi lactic acid bacteria (LAB) strains, which induced IL-10 expression in lipopolysaccharide (LPS)-stimulated peritoneal macrophages. To evaluate the inflammatory effect of G-101, we examined its inhibitory effect in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitic mice.
  
  
  RESULTS
  The colitic mice were prepared by intrarectal injection of TNBS. We measured intestinal mucosal cytokines by enzyme-linked immunosorbent assay; activation of transcription factors, by immunoblotting; and macrophage polarization markers, by real-time polymerase chain reaction. Of 200 LAB strains tested, Lact. brevis G-101 showed most potent activity for induction of IL-10 expression in LPS-stimulated peritoneal macrophages. However, it significantly inhibited the expression of TNF-α, IL-1β and IL-6 and the phosphorylation of IRAK1 and AKT, and activated NF-κB and MAPKs. Treatment with TNBS caused colon shortening; increased myeloperoxidase activity; and increased IL-1β, IL-6 and TNF-α expression in mice. Oral administration of Lact. brevis G-101 significantly inhibited these activities. Lactobacillus brevis G-101 inhibited TNBS-induced IRAK-1 phosphorylation and NF-κB activation, as well as the expression of COX-2 and iNOS. Lactobacillus brevis G-101 inhibited the expression of M1 macrophage markers, but increased the expression of M2 macrophages in the colons of TNBS-treated mice.
  
  
  CONCLUSIONS
  Lactobacillus brevis G-101 may improve colitis by inhibiting the IRAK1/NF-κB, MAPK and AKT pathways and by polarizing M1 macrophages to M2-like macrophages.
  
  
  CONCLUSIONS
  These results suggest that IL-10 expression-inducing LAB can ameliorate colitis by inhibiting NF-κB activation and macrophage polarization.
authors.affiliation: Department of Pharmacy, College of Pharmacy, Kyung Hee University, Seoul, Korea; Department of Food and Nutrition, Kyung Hee University, Seoul, Korea.
authors.forename: S-E
authors.initials: SE
authors.lastname: Jang
authors.forename: S R
authors.initials: SR
authors.lastname: Hyam
authors.forename: M J
authors.initials: MJ
authors.lastname: Han
authors.forename: S-Y
authors.initials: SY
authors.lastname: Kim
authors.forename: B-G
authors.initials: BG
authors.lastname: Lee
authors.forename: D-H
authors.initials: DH
authors.lastname: Kim
mesh_terms: D000818:Animals; D003092:Colitis / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism / Q000628:therapy*; D003106:Colon / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D016753:Interleukin-10 / Q000096:biosynthesis; D052196:Levilactobacillus brevis; D008070:Lipopolysaccharides / Q000494:pharmacology; D017737:Macrophages, Peritoneal / Q000187:drug effects / Q000276:immunology* / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000037:antagonists & inhibitors / Q000378:metabolism; D014302:Trinitrobenzenesulfonic Acid
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D016328:NF-kappa B; D016753:Interleukin-10; D014302:Trinitrobenzenesulfonic Acid; D051057:Proto-Oncogene Proteins c-akt; D020928:Mitogen-Activated Protein Kinases
keywords: IL-10; Lactobacillus brevis G-101; NF-kB; colitis; macrophage polarization