Anti-inflammatory effects of bifidobacteria by inhibition of LPS-induced NF-kappaB activation

World J Gastroenterol. 2006 Jun 21;12(23):3729-35. doi: 10.3748/wjg.v12.i23.3729.


Aim: 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).

Conclusion: Some strains of bifidobacteria are effective in inhibiting LPS-induced inflammation and thus might be appropriate candidates for probiotic intervention in chronic intestinal inflammation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bifidobacterium / genetics
  • Bifidobacterium / physiology*
  • Cyclooxygenase 2 / analysis
  • Cyclooxygenase 2 / genetics
  • Dose-Response Relationship, Drug
  • Gene Expression Regulation, Bacterial / physiology
  • Gene Expression Regulation, Neoplastic / physiology
  • Genes, Reporter / genetics
  • Genes, Reporter / physiology
  • HT29 Cells
  • Humans
  • Inflammation / drug therapy
  • Inflammation / microbiology*
  • Inflammation / physiopathology
  • Inflammation / prevention & control*
  • Intercellular Adhesion Molecule-1 / analysis
  • Intercellular Adhesion Molecule-1 / genetics
  • Interleukin-8 / genetics
  • Interleukin-8 / metabolism
  • Intestinal Mucosa / chemistry
  • Intestinal Mucosa / microbiology
  • Intestinal Mucosa / pathology
  • Intestinal Mucosa / physiopathology
  • Lipopolysaccharides / pharmacology*
  • NF-kappa B / antagonists & inhibitors*
  • NF-kappa B / drug effects*
  • NF-kappa B / genetics
  • NF-kappa B / physiology
  • Probiotics / therapeutic use
  • RNA, Messenger / analysis
  • RNA, Messenger / genetics
  • Tumor Necrosis Factor-alpha / analysis
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / pharmacology


  • Interleukin-8
  • Lipopolysaccharides
  • NF-kappa B
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
  • Cyclooxygenase 2