Immunoregulation of Murine Immunocytes to Bifidobacteria Strain Isolated from Feces of Healthy Korean Children: IL-10 Release and Proportional Change of CD4+CD25+ Cells

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).

Anti-CD3 Antibody Induces IL-10-producing CD4+CD25+ Regulatory T Cells, Which Suppress T Cell Response in Rheumatoid Arthritis Patients

BACKGROUND: Regulatory T cells (Tregs) have been investigated intensively for some decades. These cells regulate the immune system, prevent overactivated immune responses and can be used therapeutically. For rheumatoid arthritis (RA), understanding the functions and status of Tregs is an important step for understanding immune regulation in this autoimmune disease. METHODS: We investigated the percentages, phenotypes and suppressive functions of CD4+CD25+ Tregs in peripheral blood (PB) of patients with RA. RESULTS: The percentages were higher in the patients (n=12) than in healthy controls (n=10), and the cells expressed the CD45RBlow, CTLA-4 and CCR7 phenotypes. We also investigated the expression of Foxp3 and secretion of interleukin (IL)-10 induced CD4+CD25+ Tcells by anti-CD3 antibody treatment. A suppressive function of the patients' cells was shown through coculture with CD4+CD25+ T cells in vitro. CONCLUSION: We suggest that, despite their increased numbers and suppressive function, they manage the ongoing inflammation ineffectively. It might be possible to apply IL-10 to induce the proliferation of IL-10-producing Tregs as therapy for RA.