title: Oral administration of Lactobacillus plantarum K68 ameliorates DSS-induced ulcerative colitis in BALB/c mice via the anti-inflammatory and immunomodulatory activities.
abstract: Many different kinds of fermented food are consumed daily in Taiwan, such as stinky tofu, suan-tsai, and fu-tsai. We have previously reported the diversity of lactic acid bacteria (LAB) at different stages of fermentation in the production of suan-tsai and fu-tsai. In this study, the anti-inflammatory and immunomodulatory activities of Lactobacillus plantarum K68 (K68) isolated from fu-tsai were evaluated. K68 significantly inhibited the production of tumor necrosis factor-α (TNF-α) and prostaglandin E(2) (PGE(2)) in lipopolysaccharide (LPS)-induced murine macrophage RAW 264.7 cells and stimulated interferon-γ (IFN-γ) production in human peripheral blood mononuclear cells (hPBMCs). Additionally, orally administered K68 ameliorated dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in BALB/c mice. Both the disease activity index (DAI) and histological scores (HIS) showed that the severity of UC was significantly reduced by oral administration of K68. Furthermore, the production of pro inflammatory cytokines TNF-α, interleukin-1β (IL-1β), and interleukin-6 (IL-6) was significantly reduced in K68-administered group. Colonic mRNA expression levels of TNF-α, cyclooxygenase-2 (COX-2), forkhead box P3 (Foxp3), suppressors of cytokine signaling 3 (SOCS3), and toll like receptor 4 (TLR4), were also reduced in the K68-administered group. These results suggest that K68 exhibits anti-inflammatory and immunomodulatory activities that ameliorate DSS-induced experimental colitis.
authors: Institute of Biochemistry and Molecular Biology, National Yang-Ming University, No.155, Sec.2, Linong Street, Taipei, 11221 Taiwan, ROC. skywenn@gmail.com
authors: Yen-Wenn
authors: YW
authors: Liu
authors: Yu-Wen
authors: YW
authors: Su
authors: Wei-Kee
authors: WK
authors: Ong
authors: Tzu-Hao
authors: TH
authors: Cheng
authors: Ying-Chieh
authors: YC
authors: Tsai
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D002478:Cells, Cultured; D003093:Colitis, Ulcerative / Q000139:chemically induced / Q000276:immunology / Q000628:therapy*; D051546:Cyclooxygenase 2 / Q000096:biosynthesis; D016207:Cytokines / Q000096:biosynthesis; D016264:Dextran Sulfate / Q000009:adverse effects; D015232:Dinoprostone / Q000096:biosynthesis; D005260:Female; D051858:Forkhead Transcription Factors / Q000096:biosynthesis; D006801:Humans; D007155:Immunologic Factors / Q000627:therapeutic use*; D048191:Lactiplantibacillus plantarum; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism; D008070:Lipopolysaccharides / Q000378:metabolism; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D019936:Probiotics / Q000008:administration & dosage*; D012720:Severity of Illness Index; D050826:Suppressor of Cytokine Signaling Proteins / Q000096:biosynthesis; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D051858:Forkhead Transcription Factors; D007155:Immunologic Factors; D008070:Lipopolysaccharides; D050826:Suppressor of Cytokine Signaling Proteins; D051197:Toll-Like Receptor 4; D016264:Dextran Sulfate; D051546:Cyclooxygenase 2; D015232:Dinoprostone