Mannose receptor and macrophage galactose-type lectin are involved in Bordetella pertussis mast cell interaction
| Autor: | Krisztina V. Vukman, Sandra M. O’Neill, Alessandra Ravidà, Allison M. Aldridge |
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| Rok vydání: | 2013 |
| Předmět: |
Lipopolysaccharides
Bordetella pertussis T-Lymphocytes medicine.medical_treatment Immunology Asialoglycoproteins Receptors Cell Surface Biology Lymphocyte Activation Interferon-gamma Mice Immune system medicine Animals Syk Kinase Immunology and Allergy Lectins C-Type Secretion Mast Cells Egtazic Acid Interleukin-6 Tumor Necrosis Factor-alpha Toll-Like Receptors Intracellular Signaling Peptides and Proteins NF-kappa B Membrane Proteins Cell Biology Protein-Tyrosine Kinases Intercellular Adhesion Molecule-1 biology.organism_classification Mast cell Cell biology Mice Inbred C57BL Mannose-Binding Lectins Cytokine medicine.anatomical_structure Tumor necrosis factor alpha Cytokine secretion Mannose Receptor Mannose receptor |
| Zdroj: | Journal of Leukocyte Biology. 94:439-448 |
| ISSN: | 1938-3673 0741-5400 |
| DOI: | 10.1189/jlb.0313130 |
| Popis: | Mast cells are crucial in the development of immunity against Bordetella pertussis, and the function of TLRs in this process has been investigated. Here, the interaction between mast cells and B. pertussis with an emphasis on the role of CLRs is examined. In this study, two CLRs, MGL and MR, were detected for the first time on the surface of mast cells. The involvement of MR and MGL in the stimulation of mast cells by heat-inactivated BP was investigated by the use of blocking antibodies and specific carbohydrate ligands. The cell wall LOS of BP was also isolated to explore its role in this interaction. Mast cells stimulated with heat-inactivated BP or BP LOS induced TNF-α, IL-6, and IFN-γ secretion, which was suppressed by blocking MR or MGL. Inhibition of CLRs signaling during BP stimulation affected the ability of mast cells to promote cytokine secretion in T cells but had no effect on the cell-surface expression of ICAM1. Blocking MR or MGL suppressed BP-induced NF-κB expression but not ERK phosphorylation. Syk was involved in the CLR-mediated activation of mast cells by BP. Bacterial recognition by immune cells has been predominantly attributed to TLRs; in this study, the novel role of CLRs in the BP–mast cell interaction is highlighted. |
| Databáze: | OpenAIRE |
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