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092 HELICOBACTER PYLORI INDUCES ONCOSTATIN M IN THE MONOCYTIC CELL-LINE THP-1 Z Zeaiter1, M Stein1, H Diaz2, HQ Huynh3 INTRODUCTION: Helicobacter pylori is estimated to infect at least half of the world's population, and chronic, persistent infection by H. pylori may cause gastric diseases, such as chronic atrophic gastritis, peptic ulcers, mucosa-associated lymphoid tissue (MALT) lymphoma and adenocarcinoma. Oncostatin M (OSM), a member of the IL-6 subfamily, is a multifunctional cytokine produced by activated T lymphocytes and monocytes. It shares significant homology with leukemia inhibitory factor (LIF). It has a variety of biological activities depending upon cell type: i- inhibition and stimulation of cell growth, ii- cell survival, iii- induction of cell proliferation, iv- inhibition of cell differentiation, v- modulation of cellular responses and vi- wound healing.
1Department of Medical Microbiology & Immunology; 2Division of Gastroenterology, Department of Medicine; 3Division of Pediatric Gastroenterology, Department of Pediatrics, Walter Mackenzie Health Sciences Centre, University of Alberta, Calgary, Alberta
AIM: Investigation of the effect of H. pylori on signaling pathways using monocytic cell-line THP-1.
METHODS: THP-1 cultured cells were infected by H. pylori G27 for different time points; total RNA was extracted from infected and uninfected cells, reverse transcribed, labeled and hybridized to a nylon Jak/Stat oligo array. Real-time semi quantitative PCR was used to confirm the result for genes with significant expression variation. Western blot and ELISA were employed to detect OSM protein expression.
RESULTS:The expression of OSM was induced by H. pylori infection; at 2h time point the array value of OSM RNA was not detected in the uninfected but highly present in the infected. At 4h H. pylori induces OSM expression by 3.3 folds. When comparing infected samples data, OSM expression was maximum at 2h and = 2 folds the expression level at 4h. These results were confirmed by Real-time semi quantitative PCR. H. pylori induced OSM expression by 4, 10 and 6 folds at infection times 1, 2 and 4 hours, respectively. So far, OSM could not be detected in a consistent manner by Western blot and ELISA.
CONCLUSION: This is the first published report of the induction of the cytokine OSM by H. pylori to our knowledge. The role of this cytokine in the pathogenesis of H. pylori infection warrant further investigation. Potentially its role in cell proliferation and inhibition of cell differentiation may contribute to the development of MALT lymphoma and gastric adenocarcinoma in H. pylori infected individuals.