Dendritic cells express CCR7 and migrate in response to CCL19 (MIP-3beta) after exposure to Helicobacter pylori |
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| Authors: | Hansson Malin Lundgren Anna Elgbratt Kristina Quiding-Järbrink Marianne Svennerholm Ann-Mari Johansson Eva-Liz |
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| Institution: | 1. Service d’Hématologie et de Thérapie Cellulaire, CHU Haut-Lévêque, Bordeaux, France;2. Laboratoire de Parasitologie Mycologie, CHU Pellegrin, Bordeaux, France;3. Etablissement Français du Sang, Bordeaux, France;4. Université Bordeaux Segalen, Bordeaux, France;1. Division of Gastroenterology, Massachusetts General Hospital, Boston, Massachusetts;2. Harvard Medical School, Boston, Massachusetts;3. Clinical and Translational Epidemiology Unit, Massachusetts General Hospital, Boston, Massachusetts;4. National Cancer Centre Singapore, Singapore;5. Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts;6. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts;7. Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts;8. Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts;9. Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts;10. Department of Pathology, Brigham and Women’s Hospital, Boston, Massachusetts;1. Departamento de Fomento de la Producción Animal, Facultad de Ciencias Veterinarias y Pecuarias, Universidad de Chile, Santiago, Chile;2. Instituto de Bioquímica y Microbiología, Universidad Austral de Chile, Valdivia, Chile;3. Instituto de Ciencia Animal, Universidad Austral de Chile, Valdivia, Chile;4. Ross University School of Veterinary Medicine, St. Kitts, Basseterre, West Indies;1. Departments of Microbiology, Birmingham Women''s & Children''s NHS Foundation Trust, Birmingham Children''s Hospital, Steelhouse Lane, Birmingham, B4 6NH, UK;2. Departments of Facilities, Birmingham Women''s & Children''s NHS Foundation Trust, Birmingham Children''s Hospital, Steelhouse Lane, Birmingham, B4 6NH, UK;1. Upper Airways Research Laboratory, Ghent University Hospital, Ghent, Belgium;2. Department of Otorhinolaryngology, Ghent University Hospital, Ghent, Belgium;3. Randall Division of Cell and Molecular Biophysics and Division of Allergy, Asthma and Lung Biology, London, United Kingdom;4. GE01, Division of Rheumatology, Department of Internal Medicine, Ghent University Hospital, Ghent, Belgium;5. Unit for Molecular Immunology and Inflammation, Inflammation Research Center, VIB, Ghent, Belgium;6. Division of Immunopathology, Department of Pathophysiology and Allergy Research, Centre for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria;7. Department of Dermatology, Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, Brussels, Belgium;8. Center of Allergy & Environment (ZAUM), Technical University of Munich and Helmholtz Center Munich, German Research Center for Environmental Health member of the German Center for Lung Research (DZL), Munich, Germany;9. Northwestern University Feinberg School of Medicine, Chicago, Ill;10. Division of ENT Diseases, Clintec, Karolinska Institutet, Stockholm, Sweden;1. Centre for Infectious Disease Control, National Institute of Public Health and the Environment (RIVM), Bilthoven, The Netherlands;2. Department of Immunology and Infectious Diseases, Wilhelmina Children''s Hospital, University Medical Center, Utrecht, The Netherlands |
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| Abstract: | 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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