[Anti-inflammatory mechanism of Lactobacillus rhamnosus GG in lipopolysaccharide- stimulated HT-29 cell].

Sang Kil Lee, Kyung Min Yang, Jae Hee Cheon, Tae Il Kim, Won Ho Kim

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

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. HT-29 cells were stimulated with interleukin (IL)-1β (2 ng/mL), tumor necrosis factor (TNF)-α (20 ng/mL), and LPS (20 μg/mL) in the presence or absence of LGG (10 7 -10 9 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 IκBa degradation was evaluated by western blot and intranuclear translocation of NF-κB was determined by western blot and immunofluorescence. LGG did not affect the viability of HT-29 cells. Pretreatment of HT-29 cells with LGG significantly blocked TNF-α, 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-κB nuclear translocation and also blocked LPS-induced IκBα degradation. LGG also down-regulated TLR4 mRNA activated by LPS. LGG attenuates LPS induced inflammation, and this may be associated with TLR4/NF-κB down-regulation.

Original languageEnglish
Pages (from-to)86-93
Number of pages8
JournalThe Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
Volume60
Issue number2
DOIs
Publication statusPublished - 2012 Aug

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Lactobacillus rhamnosus
HT29 Cells
Lipopolysaccharides
Anti-Inflammatory Agents
Toll-Like Receptor 4
Probiotics
Interleukin-8
Messenger RNA
Tumor Necrosis Factor-alpha
Western Blotting
Inflammation
Polymerase Chain Reaction
NF-kappa B

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

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title = "[Anti-inflammatory mechanism of Lactobacillus rhamnosus GG in lipopolysaccharide- stimulated HT-29 cell].",
abstract = "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. HT-29 cells were stimulated with interleukin (IL)-1β (2 ng/mL), tumor necrosis factor (TNF)-α (20 ng/mL), and LPS (20 μg/mL) in the presence or absence of LGG (10 7 -10 9 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 IκBa degradation was evaluated by western blot and intranuclear translocation of NF-κB was determined by western blot and immunofluorescence. LGG did not affect the viability of HT-29 cells. Pretreatment of HT-29 cells with LGG significantly blocked TNF-α, 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-κB nuclear translocation and also blocked LPS-induced IκBα degradation. LGG also down-regulated TLR4 mRNA activated by LPS. LGG attenuates LPS induced inflammation, and this may be associated with TLR4/NF-κB down-regulation.",
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[Anti-inflammatory mechanism of Lactobacillus rhamnosus GG in lipopolysaccharide- stimulated HT-29 cell]. / Lee, Sang Kil; Yang, Kyung Min; Cheon, Jae Hee; Kim, Tae Il; Kim, Won Ho.

In: The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi, Vol. 60, No. 2, 08.2012, p. 86-93.

Research output: Contribution to journalArticle

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