Immunoregulation of Murine Immunocytes to Bifidobacteria Strain Isolated from Feces of Healthy Korean Children: IL-10 Release and Proportional Change of CD4+CD25+ Cells
Journal of Bacteriology and Virology
;
: 171-177, 2010.
Artigo
em Coreano
| WPRIM
| ID: wpr-69386
ABSTRACT
Bifidobacteria is one of the prototypes of probiotics bacteria, normally inhabitating the intestinal tract of humans. To search for a potent immunoregulatory Bifidobacteria strain, we screened the Bifidobacteria strains isolated from the feces of healthy Korean children. The mRNA or protein expression of an anti-inflammatory cytokine, IL-10, from mouse macrophages stimulated with live Bifidobacteria was examined. Of tested strains, Bifidobacteria A28 induced the highest IL-10 gene expression of murine macrophages. To probe immunoregulatory activity of the selected strain on the mice, we evaluated the proportional changes of CD4+CD25+ surface marker in the murine splenocytes. Flow cytometric analysis showed that the overall percentages of CD4+CD25+ cells in A28-treated splenocytes were higher than those of untreated splenocytes. In parallel, IL-10 release from A28-treated mouse peritoneal macrophages and splenocytes was significantly higher than that of untreated control cells. Collectively, the Bifidobacteria A28 strain isolated from the feces of healthy Korean children augments the mRNA or protein expression of IL-10 release from mouse peritoneal macrophages as well as the proportion of CD4+CD25+ cells of naive splenocytes. These provide in vitro scientific clues that Bifidobacteria A28 might be usable for anti-inflammatory disease such as inflammatory bowel disease (IBD).
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Entorses e Distensões
/
Bactérias
/
RNA Mensageiro
/
Doenças Inflamatórias Intestinais
/
Expressão Gênica
/
Interleucina-10
/
Macrófagos Peritoneais
/
Probióticos
/
Fezes
/
Macrófagos
Limite:
Animais
/
Humanos
Idioma:
Coreano
Revista:
Journal of Bacteriology and Virology
Ano de publicação:
2010
Tipo de documento:
Artigo
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