title: Generation of regulatory dendritic cells and CD4+Foxp3+ T cells by probiotics administration suppresses immune disorders.
abstract: The beneficial effects of probiotics have been described in many diseases, but the mechanism by which they modulate the immune system is poorly understood. In this study, we identified a mixture of probiotics that up-regulates CD4(+)Foxp3(+) regulatory T cells (Tregs). Administration of the probiotics mixture induced both T-cell and B-cell hyporesponsiveness and down-regulated T helper (Th) 1, Th2, and Th17 cytokines without apoptosis induction. It also induced generation of CD4(+)Foxp3(+) Tregs from the CD4(+)CD25(-) population and increased the suppressor activity of naturally occurring CD4(+)CD25(+) Tregs. Conversion of T cells into Foxp3(+) Tregs is directly mediated by regulatory dendritic cells (rDCs) that express high levels of IL-10, TGF-beta, COX-2, and indoleamine 2,3-dioxygenase. Administration of probiotics had therapeutical effects in experimental inflammatory bowel disease, atopic dermatitis, and rheumatoid arthritis. The therapeutical effect of the probiotics is associated with enrichment of CD4(+)Foxp3(+) Tregs in the inflamed regions. Collectively, the administration of probiotics that enhance the generation of rDCs and Tregs represents an applicable treatment of inflammatory immune disorders.
authors.affiliation: Department of Life Sciences, Gwangju Institute of Science and Technology, Gwangju 500-712, Korea.
authors.forename: Ho-Keun
authors.initials: HK
authors.lastname: Kwon
authors.forename: Choong-Gu
authors.initials: CG
authors.lastname: Lee
authors.forename: Jae-Seon
authors.initials: JS
authors.lastname: So
authors.forename: Chang-Suk
authors.initials: CS
authors.lastname: Chae
authors.forename: Ji-Sun
authors.initials: JS
authors.lastname: Hwang
authors.forename: Anupama
authors.initials: A
authors.lastname: Sahoo
authors.forename: Jong Hee
authors.initials: JH
authors.lastname: Nam
authors.forename: Joon Haeng
authors.initials: JH
authors.lastname: Rhee
authors.forename: Ki-Chul
authors.initials: KC
authors.lastname: Hwang
authors.forename: Sin-Hyeog
authors.initials: SH
authors.lastname: Im
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D001169:Arthritis, Experimental / Q000276:immunology / Q000473:pathology / Q000628:therapy; D039521:CD11c Antigen / Q000378:metabolism; D003713:Dendritic Cells / Q000276:immunology* / Q000473:pathology; D003876:Dermatitis, Atopic / Q000276:immunology / Q000473:pathology / Q000628:therapy; D004195:Disease Models, Animal; D051858:Forkhead Transcription Factors / Q000378:metabolism*; D007154:Immune System Diseases / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D007165:Immunosuppression Therapy; D015212:Inflammatory Bowel Diseases / Q000276:immunology / Q000473:pathology / Q000628:therapy; D051379:Mice; D008807:Mice, Inbred BALB C; D008822:Mice, Transgenic; D019936:Probiotics / Q000008:administration & dosage*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000378:metabolism / Q000473:pathology
chemical_list: D039521:CD11c Antigen; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse