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KMID : 0614620120600020086
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Korean Journal of Gastroenterology
2012 Volume.60 No. 2 p.86 ~ p.93
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Anti-inflammatory Mechanism of Lactobacillus rhamnosus GG in Lipopolysaccharidestimulated HT-29 Cell
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Lee Sang-Kil
Yang Kyoung-Min
Cheon Jae-Hee
Kim Tae-Il
Kim Won-Ho
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Abstract
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Background/Aims: Probiotics are live non-pathogenic organisms that belong to the resident microflora, and confer health benefits by multiple mechanisms. Lactobacillus rhamnosus GG (LGG) is one of the probiotic bacteria that ameliorates intestinal injury and inflammation caused by various stimuli. We aimed to evaluate the anti-inflammatory effect and mechanism of LGG in lipopolysaccharide (LPS)-stimulated HT-29 cells.
Methods: HT-29 cells were stimulated with interleukin (IL)-1b (2 ng/mL), tumor necrosis factor (TNF)-a (20 ng/mL), and LPS (20 mg/mL) in the presence or absence of LGG (107-109 colony forming units/mL). Production of the pro-inflammatory chemokine IL-8 was measured by ELISA and semi-quantitative PCR. Transcriptional activity of NF-kB-responsive gene was evaluated by luciferase assay with reporter gene. Toll-like receptor 4 (TLR4) mRNA expression was assessed by semi-quantitative PCR. The IkBa degradation was evaluated by western blot and intranuclear translocation of NF-kB was determined by western blot and immunofluorescence.
Results: LGG did not affect the viability of HT-29 cells. Pretreatment of HT-29 cells with LGG significantly blocked TNF-a, and LPS induced IL-8 activation at both mRNA and protein level (p＜0.05). Pretreatment of HT-29 cells with LGG attenuated LPS-induced NF-kB nuclear translocation and also blocked LPS-induced IkBa degradation. LGG also down-regulated TLR4 mRNA activated by LPS.
Conclusions: LGG attenuates LPS induced inflammation, and this may be associated with TLR4/NF-kB down-regulation.
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KEYWORD
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Lactobacillus rhamnosus, Lipopolysaccharides, NF-κB
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