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This Article Full Text (Papers in Press[PDF]) All Versions of this Article: jmm.0.009407-0v1 58/8/996    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Ryan, K. A Articles by O'Toole, P. W. PubMed PubMed Citation Articles by Ryan, K. A Articles by O'Toole, P. W. Agricola Articles by Ryan, K. A Articles by O'Toole, P. W.

Lactobacillus salivarius modulates cytokine induction and virulence factor gene expression in Helicobacter pylori

¹ Univ College Cork;

² NUI Galway;

³ University College Cork

⁴ E-mail: pwotoole{at}ucc.ie

Received January 12, 2009
Accepted April 27, 2009

Human infection by the gastric pathogen Helicobacter pylori is characterized by a robust immune response which rarely prevents persistent H. pylori colonization. Emerging evidence suggests that lactobacilli may reduce H. pylori infection rates and associated inflammation. In this study we measured the ability of two model strains of Lactobacillus salivarius (UCC118 and UCC119) to modulate gastric epithelial cell chemokine responses to H. pylori infection. Pre-treatment of AGS cells with either L. salivarius strain significantly decreased interleukin-8 (IL-8) production upon exposure to H. pylori, but not in cells stimulated with TNF-. The production of the chemokines CCL20 and IP-10 by AGS cells infected with H. pylori was also altered following pre-treatment with UCC118 and UCC119. We show a greater reduction in IL-8 production with UCC119 was due to the production of more acid by this strain. Futhermore, UV-killed cells of both lactobacillus strains were still able to reduce H. pylori-induced IL-8 in the absence of acid production, indicating the action of a second anti-inflammatory mechanism. This immunomodulatory activity was not dependent on adhesion to epithelial cells or bacteriocin production. Real-time RT-PCR analysis showed that expression of eight of twelve Cag pathogenicity island genes tested was down-regulated by exposure to L. salivarius, but not by cells of four other lactobacillus species. CagA accumulated in H. pylori cells following exposure to L. salivarius presumably as a result of loss of functionality of the Cag secretion system. These data identify a new mechanism whereby some probiotic bacteria have a positive affect on H. pylori-associated inflammation without clearing the infection.