title: Lactococcus lactis subsp. cremoris FC alleviates symptoms of colitis induced by dextran sulfate sodium in mice.
abstract: Probiotics have been used to treat human gastrointestinal inflammations including inflammatory bowel disease (IBD). However, the exact mechanisms by which probiotics act to protect against intestinal inflammation have yet to be fully elucidated. The aim of this study was to evaluate anti-inflammatory effects of Lactococcus lactis subsp. cremoris FC using in vivo and in vitro inflammation models. Colitis was induced in C57BL/6 mice by administration of 3% dextran sulfate sodium to drinking water. In the cellular level assessment, a gut inflammation model with the co-culture system consisting Caco-2 cells and RAW264.7 cells stimulated by LPS was used. Administration of L. lactis subsp. cremoris FC significantly ameliorated shortening of colon length and histological score of the colon in DSS-induce colitis mice. In addition, the treatment of L. lactis subsp. cremoris FC improved the aberrant mRNA expression in inflamed tissue near to control level through notable suppression of TNF-alpha (P<0.05), IFN-gamma (P<0.05), IL-6, iNOS, and MIP-2 mRNA expression. In addition, in a gut inflammation model, treatment with L. lactis subsp. cremoris FC resulted in significant down-regulation of IL-8 mRNA expression in Caco-2 cells and inhibition of NF-kappaB nuclear translocation in RAW264.7 cells. Our findings indicate that administration of L. lactis subsp. cremoris FC improves negative effects of DSS-induced colitis in mice through the inhibition of inflammatory cell infiltration.
authors.affiliation: Organization of Advanced Science and Technology, Kobe University, 1-1 Rokkodai-cho, Nada-ku, Kobe 657-8501, Japan. nishitani@people.kobe-u.ac.jp
authors.forename: Yosuke
authors.initials: Y
authors.lastname: Nishitani
authors.forename: Takeshi
authors.initials: T
authors.lastname: Tanoue
authors.forename: Katsushige
authors.initials: K
authors.lastname: Yamada
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Ishida
authors.forename: Masaru
authors.initials: M
authors.lastname: Yoshida
authors.forename: Takeshi
authors.initials: T
authors.lastname: Azuma
authors.forename: Masashi
authors.initials: M
authors.lastname: Mizuno
mesh_terms: D000818:Animals; D018938:Caco-2 Cells; D003092:Colitis / Q000139:chemically induced / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology / Q000628:therapy*; D003106:Colon / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D016207:Cytokines / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D016264:Dextran Sulfate / Q000008:administration & dosage; D020895:Enterocytes / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D056747:Immunomodulation; D015212:Inflammatory Bowel Diseases / Q000276:immunology / Q000382:microbiology / Q000628:therapy; D013294:Lactococcus lactis / Q000276:immunology*; D008070:Lipopolysaccharides / Q000378:metabolism; D008264:Macrophages / Q000276:immunology / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000276:immunology / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D019936:Probiotics / Q000008:administration & dosage* / Q000494:pharmacology
chemical_list: D016207:Cytokines; D008070:Lipopolysaccharides; D016328:NF-kappa B; D016264:Dextran Sulfate; D052247:Nitric Oxide Synthase Type II