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

被引:141
作者
Riedel, Christian U. [1 ]
Foata, Francis
Philippe, David
Adolfsson, Oskar
Eikmanns, Bernhard J.
Blum, Stephanie
机构
[1] Natl Univ Ireland Univ Coll Cork, Dept Microbiol, Cork, Ireland
[2] Univ Ulm, Dept Microbiol & Biotechnol, D-89068 Ulm, Germany
[3] Nestle Res Ctr, Immunol Grp, Nutr & Hlth Dept, CH-1026 Lausanne, Switzerland
关键词
NF-kappa B; bifidobacteria; anti-inflammatory; LPS;
D O I
10.3748/wjg.v12.i23.3729
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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-kappa B 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 kappa B (NF-kappa B) indicating that bifidobacteria themselves do not induce inflammatory events in IECs. However, six out of eight bifidobacteria tested inhibited lipopolysaccharide-(LPS-) induced NF-kappa B activation in a close- and strain-dependent manner. In contrast, NF-kappa B 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-incluced inhibition of NF-kappa B 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-incluced inflammation and thus might be appropriate candidates for probiotic intervention in chronic intestinal inflammation. (c) 2006 The WJG Press. All rights reserved.
引用
收藏
页码:3729 / 3735
页数:7
相关论文
共 57 条
[1]   TLR signaling in the gut in health and disease [J].
Abreu, MT ;
Fukata, M ;
Arditi, M .
JOURNAL OF IMMUNOLOGY, 2005, 174 (08) :4453-4460
[2]   Toll-like receptor signalling [J].
Akira, S ;
Takeda, K .
NATURE REVIEWS IMMUNOLOGY, 2004, 4 (07) :499-511
[3]   Probiotic bifidobacteria protect mice from lethal infection with shiga toxin-producing Escherichia coli O157:H7 [J].
Asahara, T ;
Shimizu, K ;
Nomoto, K ;
Hamabata, T ;
Ozawa, A ;
Takeda, Y .
INFECTION AND IMMUNITY, 2004, 72 (04) :2240-2247
[4]   Increased resistance of mice to Salmonella enterica serovar Typhimurium infection by synbiotic administration of Bifidobacteria and transgalactosylated oligosaccharides [J].
Asahara, T ;
Nomoto, K ;
Shimizu, K ;
Watanuki, M ;
Tanaka, R .
JOURNAL OF APPLIED MICROBIOLOGY, 2001, 91 (06) :985-996
[5]   Mechanisms of disease - Nuclear factor-kappa b - A pivotal transcription factor in chronic inflammatory diseases [J].
Barnes, PJ ;
Larin, M .
NEW ENGLAND JOURNAL OF MEDICINE, 1997, 336 (15) :1066-1071
[6]   ADHESION OF HUMAN BIFIDOBACTERIAL STRAINS TO CULTURED HUMAN INTESTINAL EPITHELIAL-CELLS AND INHIBITION OF ENTEROPATHOGEN-CELL INTERACTIONS [J].
BERNET, MF ;
BRASSART, D ;
NEESER, JR ;
SERVIN, AL .
APPLIED AND ENVIRONMENTAL MICROBIOLOGY, 1993, 59 (12) :4121-4128
[7]   VSL#3 probiotic-mixture induces remission in patients with active ulcerative colitis [J].
Bibiloni, R ;
Fedorak, RN ;
Tannock, GW ;
Madsen, KL ;
Gionchetti, P ;
Campieri, M ;
De Simone, C ;
Sartor, RB .
AMERICAN JOURNAL OF GASTROENTEROLOGY, 2005, 100 (07) :1539-1546
[8]   The immunological and genetic basis of inflammatory bowel disease [J].
Bouma, G ;
Strober, W .
NATURE REVIEWS IMMUNOLOGY, 2003, 3 (07) :521-533
[9]   The role of probiotic cultures in the prevention of colon cancer [J].
Brady, LJ ;
Gallaher, DD ;
Busta, FF .
JOURNAL OF NUTRITION, 2000, 130 (02) :410S-414S
[10]   Differential alteration in intestinal epithelial cell expression of Toll-like receptor 3 (TLR3) and TLR4 in inflammatory bowel disease [J].
Cario, E ;
Podolsky, DK .
INFECTION AND IMMUNITY, 2000, 68 (12) :7010-7017