Suppression of Helicobacter pylori-induced interleukin-8 production in vitro and within the gastric mucosa by a live Lactobacillus strain

  1. Akira Tamura1,3,
  2. Hideshi Kumai3,
  3. Noboru Nakamichi3,
  4. Toshirou Sugiyama4,
  5. Ryozo Deguchi2,
  6. Atsusi Takagi2,
  7. Yasuhiro Koga1,*

Article first published online: 18 APR 2006

DOI: 10.1111/j.1440-1746.2006.04318.x

Issue

Journal of Gastroenterology and Hepatology

Journal of Gastroenterology and Hepatology

Volume 21, Issue 9, pages 1399–1406, September 2006

Additional Information

How to Cite

Tamura, A., Kumai, H., Nakamichi, N., Sugiyama, T., Deguchi, R., Takagi, A. and Koga, Y. (2006), Suppression of Helicobacter pylori-induced interleukin-8 production in vitro and within the gastric mucosa by a live Lactobacillus strain. Journal of Gastroenterology and Hepatology, 21: 1399–1406. doi: 10.1111/j.1440-1746.2006.04318.x

Author Information

  1. 1

    Laboratory for Infectious Diseases and

  2. 2

    Department of Internal Medicine, Tokai University Medical Shool, Bohseidai, Isehara,

  3. 3

    Food Functionality Research Institute, Meiji Dairies Corporation, Odawara, and

  4. 4

    Department of Gastroenterology, Hokkaido University Graduate School of Medicine, Kita, Sapporo, Japan

*Yasuhiro Koga, Laboratory for Infectious Diseases, Tokai University Medical School, Bohseidai, Isehara, Kanagawa 259-1193, Japan. Email: yasuhiro@is.icc.u-tokai.ac.jp

Publication History

  1. Issue published online: 28 JUL 2006
  2. Article first published online: 18 APR 2006
  3. Accepted for publication 14 July 2005.

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Keywords:

  • H. pylori;
  • IL-8;
  • Lactobacillus;
  • probiotics;
  • stomach

Abstract

Background:  Accumulating evidence indicates that interleukin-8 (IL-8) plays a major role in the mucosal inflammation caused by Helicobacter pylori infection. The purpose of the present study was to examine whether Lactobacillus gasseri OLL2716 (LG21) can inhibit the H. pylori-induced production of IL-8.

Methods:  A coculture system including MKN45 cells, H. pylori, and LG21 was established for an in vitro analysis. Biopsy specimens were obtained from H. pylori-infected human subjects consisting of 19 men and six women.

Results:  When LG21 was 1/100 less than H. pylori in a coculture system, LG21 significantly suppressed both the IL-8 mRNA and protein generation in the coculture. Live, but not heat- or UV-treated LG21, could exert the suppressive effect. However, this amount of LG21 could not suppress either the adhesion of H. pylori to the cell surface or the IL-8 production by tumor necrosis factor-α, which induces IL-8 generation through the activation of the transcription. These results thus suggest that LG21 suppresses an event leading to IL-8 production, which is specific for H. pylori-induced IL-8 generation, and this event is located upstream from the IL-8 transcription but downstream from the adhesion. The measurement of the IL-8 level using gastric biopsy specimens from H. pylori-infected subjects demonstrated that LG21 also suppresses the production of IL-8 in the gastric mucosa.

Conclusions:  Live LG21 were found to suppress H. pylori-induced IL-8 production in both a gastric cell line and within gastric mucosa.

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