Supernatant of Bifidobacterium breve induces dendritic cell maturation, activation, and survival through a Toll-like receptor 2 pathway
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 betwee...
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Veröffentlicht in: | Journal of Allergy and Clinical Immunology 2006-03, Vol.117 (3), p.696-702 |
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Zusammenfassung: | 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.
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).
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.
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 κB 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.
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
H1 response and control the excessive T
H2 polarization observed in atopic newborns. |
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ISSN: | 0091-6749 1097-6825 1365-2567 |
DOI: | 10.1016/j.jaci.2005.10.043 |