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Dendritic cells express CCR7 and migrate in response to CCL19 (MIP-3beta) after exposure to Helicobacter pylori

Review article
Authors Malin Hansson
Anna Lundgren
Kristina Elgbratt
Marianne Quiding-Järbrink
Ann-Mari Svennerholm
Eva-Liz Johansson
Published in Microbes Infect
Volume 8
Issue 3
Pages 841-50
Publication year 2006
Published at Institute of Biomedicine, Department of Microbiology and Immunology
Pages 841-50
Language en
Keywords CD4-Positive T-Lymphocytes/metabolism, Cell Movement/*physiology, Cell Proliferation, Chemokines, CC/genetics/*metabolism, Dendritic Cells/*metabolism, Gene Expression Regulation, Helicobacter Infections/microbiology, Helicobacter pylori/*metabolism, Humans, Receptors, CXCR4/metabolism, Receptors, Chemokine/genetics/*metabolism, Virulence Factors/metabolism
Subject categories Medical and Health Sciences


Helicobacter pylori infection induces chronic inflammation in the gastric mucosa with a marked increase in the number of lymphoid follicles consisting of infiltrating B and T cells, neutrophils, dendritic cells (DC) and macrophages. It has been suggested that an accumulation of mature DC in the tissue, resulting from a failure of DC to migrate to lymph nodes, may contribute to this chronic inflammation. Migration of DC to lymph nodes is regulated by chemokine receptor CCR7, expressed on mature DC, and the CCR7 ligands CCL19 and CCL21. In this study we analysed the maturation, in vitro migration and cytokine production of human DC after stimulation with live H. pylori. For comparison, DC responses to non-pathogenic Escherichia coli bacteria were also evaluated. Stimulation with H. pylori induced maturation of DC, i.e. up-regulation of the chemokine receptors CCR7 and CXCR4 and the maturation markers HLA-DR, CD80 and CD86. The H. pylori-stimulated DC also induced CD4(+) T-cell proliferation. DC stimulated with H. pylori secreted significantly more interleukin (IL)-12 compared to DC stimulated with E. coli, while E. coli-stimulated DC secreted more IL-10. Despite low surface expression of CCR7 protein following stimulation with H. pylori compared to E. coli, the DC migrated equally well towards CCL19 after stimulation with both bacteria. Thus, we could not detect any failure in the migration of H. pylori stimulated DC in vitro that may contribute to chronic gastritis in vivo, and our results suggest that H. pylori induces maturation and migration of DC to lymph nodes where they promote T cell responses.

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