title: Anti-inflammatory properties of intestinal Bifidobacterium strains isolated from healthy infants.
abstract: Certain Bifidobacterium strains have been shown to inhibit inflammatory responses in intestinal epithelial cells. However, the precise mechanisms of these effects, including the chemical nature of the active compounds, remain to be elucidated. Here partial characterization of the anti-inflammatory properties of Bifidobacterium strains isolated from feces of healthy infants is reported. It was found that conditioned media (CM) of all strains studied are capable of attenuating tumor necrosis factor-α (TNF-α) and lipopolysaccharide- (LPS) induced inflammatory responses in the HT-29 cell line. In contrast, neither killed bifidobacterial cells, nor cell-free extracts showed such activities. Further investigations resulted in attribution of this activity to heat-stable, non-lipophilic compound(s) resistant to protease and nuclease treatments and of molecular weight less than 3 kDa. The anti-inflammatory effects were dose- and time-dependent and associated with inhibition of IκB phosphorylation and nuclear factor-κ light chain enhancer of activated B cells (NF-κB)-dependent promoter activation. The combined treatments of cells with CMs and either LPS or TNF-α, but not with CMs alone, resulted in upregulation of transforming growth factor-β1, IκBζ, and p21(CIP) mRNAs. Our data suggest certain species-specificities of the anti-inflammatory properties of bifidobacteria. This observation should prompt additional validation studies using larger set of strains and employing the tools of comparative genomics.
authors: Department of Microbiology and Virology, Russian State Medical University, Moscow, Russia.
authors: Ekaterina V
authors: EV
authors: Khokhlova
authors: Vladimir V
authors: VV
authors: Smeianov
authors: Boris A
authors: BA
authors: Efimov
authors: Lyudmila I
authors: LI
authors: Kafarskaia
authors: Svetlana I
authors: SI
authors: Pavlova
authors: Andrei N
authors: AN
authors: Shkoporov
mesh_terms: D017209:Apoptosis; D001644:Bifidobacterium / Q000235:genetics / Q000276:immunology* / Q000302:isolation & purification*; D017077:Culture Media, Conditioned / Q000494:pharmacology; D004306:Dose-Response Relationship, Immunologic; D004926:Escherichia coli / Q000235:genetics / Q000378:metabolism; D005243:Feces / Q000382:microbiology; D015964:Gene Expression Regulation, Bacterial; D019073:HT29 Cells; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism; D007223:Infant; D007249:Inflammation / Q000139:chemically induced / Q000382:microbiology*; D016209:Interleukin-8 / Q000378:metabolism; D007422:Intestines / Q000382:microbiology*; D008070:Lipopolysaccharides / Q000009:adverse effects; D008970:Molecular Weight; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000276:immunology / Q000378:metabolism; D010766:Phosphorylation; D011401:Promoter Regions, Genetic; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013045:Species Specificity; D013997:Time Factors; D015533:Transcriptional Activation; D014162:Transfection; D016211:Transforming Growth Factor alpha / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000494:pharmacology
chemical_list: D017077:Culture Media, Conditioned; D020672:I-kappa B Proteins; D016209:Interleukin-8; D008070:Lipopolysaccharides; D016328:NF-kappa B; C000606204:NFKBIA protein, human; D012333:RNA, Messenger; D016211:Transforming Growth Factor alpha; D014409:Tumor Necrosis Factor-alpha; D000072000:NF-KappaB Inhibitor alpha