Anti-inflammatory effects of bifidobacteria by inhibition of LPS-induced NF-kappaB activation.
OBJECTIVE
Different strains of bifidobacteria were analysed for their effects on HT-29 intestinal epithelial cells (IECs) in in vitro models both of the non-inflamed and inflamed intestinal epithelium.


METHODS
A reporter gene system in HT-29 cells was used to measure levels of NF-kappaB activation after challenge with bifidobacteria or after bacterial pre-treatment following LPS challenge. IL-8 protein and pro-inflammatory gene expression was investigated using normal HT-29 cells.


RESULTS
None of the bifidobacteria tested induced activation of nuclear factor kappaB (NF-kappaB) indicating that bifidobacteria themselves do not induce inflammatory events in IECs. However, six out of eight bifidobacteria tested inhibited lipopolysaccharide- (LPS-) induced NF-kappaB activation in a dose- and strain-dependent manner. In contrast, NF-kappaB activation in response to challenge with tumor necrosis factor-alpha (TNF-alpha) was affected by none of the tested bifidobacteria, indicating that the inhibitory effect of bifidobacteria is specific for LPS-induced inflammation in IECs. As shown with two of the six inhibition-positive bifidobacteria, LPS-induced inhibition of NF-kappaB activation was accompanied by a dose-dependent decrease of interleukin 8 (IL-8) secretion and by lower mRNA levels for IL-8, TNF-alpha, cyclooxygenase 2 (Cox-2), and intercellular adhesion molecule 1 (ICAM-1).


CONCLUSIONS
Some strains of bifidobacteria are effective in inhibiting LPS-induced inflammation and thus might be appropriate candidates for probiotic intervention in chronic intestinal inflammation.
Riedel
Christian-U
CU
Department of Microbiology and Biotechnology, University of Ulm, Germany. c.riedel@ucc.ie
Foata
Francis
F
Philippe
David
D
Adolfsson
Oskar
O
Eikmanns
Bernhard-J
BJ
Blum
Stephanie
S
D001644:Bifidobacterium / Q000235:genetics / Q000502:physiology*; D051546:Cyclooxygenase 2 / Q000032:analysis / Q000235:genetics; D004305:Dose-Response Relationship, Drug; D015964:Gene Expression Regulation, Bacterial / Q000502:physiology; D015972:Gene Expression Regulation, Neoplastic / Q000502:physiology; D017930:Genes, Reporter / Q000235:genetics / Q000502:physiology; D019073:HT29 Cells; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000382:microbiology* / Q000503:physiopathology / Q000517:prevention & control*; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis / Q000235:genetics; D016209:Interleukin-8 / Q000235:genetics / Q000378:metabolism; D007413:Intestinal Mucosa / Q000737:chemistry / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000187:drug effects* / Q000235:genetics / Q000502:physiology; D019936:Probiotics / Q000627:therapeutic use; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000235:genetics / Q000494:pharmacology
D016209:Interleukin-8; D008070:Lipopolysaccharides; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D051546:Cyclooxygenase 2