Journal of Microbiology and Biotechnology

The Korean Society for Microbiology and Biotechnology (한국미생물·생명공학회)
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Lactobacillus acidophilus Strain Suppresses the Transcription of Proinflammatory-Related Factors in Human HT-29 Cells

  • Chen, Kun (Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education, College of Bioengineering, Tianjin University of Science and Technology) ;
  • Liang, Nailong (Medical Institute, Liaocheng Vocational and Technical College) ;
  • Luo, Xuegang (Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education, College of Bioengineering, Tianjin University of Science and Technology) ;
  • Zhang, Tong-Cun (Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education, College of Bioengineering, Tianjin University of Science and Technology)
  • Received : 2012.08.30
  • Accepted : 2012.09.04
  • Published : 2013.01.28
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Abstract

Previous studies have shown that lactic acid bacteria can inhibit inflammatory responses, but the mechanisms are very little known. In this study, transaction and expression of three proinflammatory factors, iNOS, PTGS-2, and IL8, which are closely related to the inflammatory response, were investigated by luciferase reporter assay and RTPCR in HT-29 cells treated by Lactobacillus acidophilus. The results showed that the live L. acidophilus sharply down-regulated the transcription of these three genes. Because there was a NF-${\kappa}B$ binding site located at -265 bp, -225 bp, and -95 bp upstream of the iNOS, PTGS-2, and IL8 promoters, respectively, we further addressed the effects of NF-${\kappa}B$ on transaction of the three promoters by cotransfection. As was expected, NF-${\kappa}Bs$ remarkably upregulated the activity of the reporter gene and, no effect of NF-${\kappa}B$s on IL-8 promoter transaction was found after NF-${\kappa}B$ binding site mutation of the IL8 promoter in HT-29 cells. In conclusion, the live L. acidophilus decreased the transcriptional activity of NF-${\kappa}B$ and, in turn, inhibited the transaction of NF-${\kappa}B$ on the three proinflammatory factors mentioned above.

Keywords

References

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