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Objectives  Soluble factors released by  Bifidobacterium breve  C50 ( Bb ) alleviate the secretion of pro-inflammatory cytokines by immune cells, but their effect on intestinal epithelium remains elusive. To decipher the mechanisms accounting for the cross-talk between bacteria/soluble factors and intestinal epithelium, we measured the capacity of the bacteria, its conditioned medium ( Bb -CM) and other Gram(+) commensal bacteria to dampen inflammatory chemokine secretion.    Methods  TNFα-induced chemokine (CXCL8) secretion and alteration of NF-κB and AP-1 signalling pathways by  Bb  were studied by EMSA, confocal microscopy and western blotting. Anti-inflammatory capacity was also tested  in vivo  in a model of TNBS-induced colitis in mice.    Results    Bb  and  Bb-CM , but not other commensal bacteria, induced a time and dose-dependent inhibition of CXCL8 secretion by epithelial cells driven by both AP-1 and NF-κB transcription pathways and implying decreased phosphorylation of p38-MAPK and IκB-α molecules. In TNBS-induced colitis in mice,  Bb -CM decreased the colitis score and inflammatory cytokine expression, an effect reproduced by dendritic cell conditioning with  Bb -CM.    Conclusions    Bb  and secreted soluble factors contribute positively to intestinal homeostasis by attenuating chemokine production. The results indicate that  Bb  down regulate inflammation at the epithelial level by inhibiting phosphorylations involved in inflammatory processes and by protective conditioning of dendritic cells.

Mechanisms Involved in Alleviation of Intestinal Inflammation by Bifidobacterium Breve Soluble Factors