4.7 Article

Supernatant of Bifidobacterium breve induces dendritic cell maturation, activation, and survival through a Toll-like receptor 2 pathway

Journal

JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 117, Issue 3, Pages 696-702

Publisher

MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2005.10.043

Keywords

Bifidobacterium breve; dendritic cells; maturation; cell survival; tolerance; Bcl-2 protein family; Toll-like receptor 2; IL-10; IL-12; allergy

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Background: Commensal gut bacteria are essential for the development and maintenance of the gut's immune system. Some bacteria strains, such as Lactobacillus and Bifidobacterium species, have been reported to provide protection from allergic and inflammatory bowel diseases. However, the interactions between these commensal bacteria and the immune system are largely unknown. Objective: We studied the effects of a supernatant from the culture of B breve C50 (BbC50) on the maturation, activation, and survival of human dendritic cells (DCs). Methods: DCs were differentiated from human monocytes with IL-4 and GM-CSF for 5 days and cultured with BbC50 supernatant (BbC50(SN)) or LPS for 2 days. Results: BbC50(SN) induced DC maturation, with increase in CD83, CD86, and HLA-DR expression. We also showed, for the first time,, that BbC50(SN) prolonged DC survival, with high IL-10 and low IL-12 production compared with that seen in LPS-DCs. Moreover, BbC50(SN) inhibited the effects of LPS on DCs, both in terms of IL-12 production and in terms of survival. The prolonged DC survival was independent of IL-10 production and nuclear factor kappa B pathway but was associated with an upregulation of Bcl-x(L) and Phospho-Bad. Finally, BbC50(SN) induced activation of Toll-like receptor 2 (TLR2)-transfected cells in contrast to TLR4-, TLR7-, and TLR9-transfected cells. Conclusion: The supernatant of B breve C50 can induce DC maturation and prolonged DC survival through TLR2, with high IL-10 production. These properties might correspond to a regulatory DC profile, which could limit the excessive T(H)1 response and control the excessive T(H)2 polarization observed in atopic newborns.

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