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 repor...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-KB 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 inhibitionpositive 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.展开更多
文摘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-KB 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 inhibitionpositive 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.
