Basic Research
Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jun 21, 2006; 12(23): 3729-3735
Published online Jun 21, 2006. doi: 10.3748/wjg.v12.i23.3729
Anti-inflammatory effects of bifidobacteria by inhibition of LPS-induced NF-κB activation
Christian U Riedel, Francis Foata, David Philippe, Oskar Adolfsson, Bernhard J Eikmanns, Stephanie Blum
Christian U Riedel, Bernhard J Eikmanns, Department of Microbiology and Biotechnology, University of Ulm, 89068 Ulm, Germany
Christian U Riedel, Francis Foata, David Philippe, Oskar Adolfsson, Stephanie Blum, Immunology Group, Nutrition and Health Dept., Nestlé Research Center, PO Box 44, CH-1026 Lausanne, Switzerland
Correspondence to: Christian U Riedel, Microbiology Department and Alimentary Pharmabiotic Centre, University College Cork, Cork, Ireland. c.riedel@ucc.ie
Telephone: +353-21-4901388 Fax: +353-21-4903101
Received: November 17, 2005
Revised: November 28, 2005
Accepted: January 14, 2006
Published online: June 21, 2006
Abstract

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-κB 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 κB (NF-κB) indicating that bifidobacteria themselves do not induce inflammatory events in IECs. However, six out of eight bifidobacteria tested inhibited lipopolysaccharide- (LPS-) induced NF-κB activation in a dose- and strain-dependent manner. In contrast, NF-κB activation in response to challenge with tumor necrosis factor-α (TNF-α) 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-κB activation was accompanied by a dose-dependent decrease of interleukin 8 (IL-8) secretion and by lower mRNA levels for IL-8, TNF-α, 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.

Keywords: NF-κB; Bifidobacteria; Anti-inflammatory; LPS