Journal article
Helicobacter pylori VacA suppresses Lactobacillus acidophilus-induced interferon beta signaling in macrophages via alterations in the endocytic pathway
G Weiss, S Forster, A Irving, M Tate, RL Ferrero, P Hertzog, H Frøkiær, M Kaparakis-Liaskos
Mbio | AMER SOC MICROBIOLOGY | Published : 2013
Abstract
Helicobacter pylori causes chronic gastritis and avoids elimination by the immune system of the infected host. The commensal bacterium Lactobacillus acidophilus has been suggested to exert beneficial effects as a supplement during H. pylori eradication therapy. In the present study, we applied whole-genome microarray analysis to compare the immune responses induced in murine bone marrow-derived macrophages (BMDMs) stimulated with L. acidophilus, H. pylori, or both bacteria in combination. While L. acidophilus induced a Th1-polarizing response characterized by high expression of interferon beta (IFN-β) and interleukin 12 (IL-12), H. pylori strongly induced the innate cytokines IL-1β and IL-1α..
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Funding Acknowledgements
Gudrun Weiss was supported by a postdoctoral fellowship and a travel grant to visit Australia from the University of Copenhagen, the Augustinus Foundation, the A.P. Mollers and Wife Chastine Mc-Kinney Mollers Foundation for Medical Science Promotion, the Christian and Ottilia Brorsons Travel Foundation for Young Scientists, the Sophus Jacobsen and Wife Astrid Jacobsens Foundation, the Oticon Foundation, and the Torben and Alice Frimodts Foundation. This work was also supported by funding from the Australian Research Council (to M. K.-L.), Victorian Life Sciences Computation Initiative, Monash e-Research, the National Health & Medical Research Council (NH&MRC) of Australia (to R. L. F. and P. H.), and the Victorian Government's Operational Infrastructure Support Program. R. L. F. and P. H. are senior and professorial research fellows, respectively, of the NH&MRC.