| Author |
Al-Afif, Ayham Alyazidi, Raidan Oldford, Sharon A. Huang, Yan Y. King, Christine A. Marr, Nico Haidl, Ian D. Anderson, Robert Marshall, Jean S. |
| Description |
Country affiliation: Canada Author Affiliation: Al-Afif A ( Department of Microbiology and Immunology, Dalhousie Inflammation Group, Dalhousie University, Halifax, Nova Scotia, Canada.); Alyazidi R ( Department of Microbiology and Immunology, Dalhousie Inflammation Group, Dalhousie University, Halifax, Nova Scotia, Canada); Oldford SA ( Department of Microbiology and Immunology, Dalhousie Inflammation Group, Dalhousie University, Halifax, Nova Scotia, Canada.); Huang YY ( Department of Microbiology and Immunology, Dalhousie Inflammation Group, Dalhousie University, Halifax, Nova Scotia, Canada); King CA ( Department of Microbiology and Immunology, Dalhousie Inflammation Group, Dalhousie University, Halifax, Nova Scotia, Canada.); Marr N ( Canadian Center for Vaccinology, Izaak Walter Killam Health Centre, Halifax, Nova Scotia, Canada.); Haidl ID ( Department of Microbiology and Immunology, Dalhousie Inflammation Group, Dalhousie University, Halifax, Nova Scotia, Canada.); Anderson R ( Department of Microbiology and Immunology, Dalhousie Inflammation Group, Dalhousie University, Halifax, Nova Scotia, Canada); Marshall JS ( Department of Microbiology and Immunology, Dalhousie Inflammation Group, Dalhousie University, Halifax, Nova Scotia, Canada) |
| Abstract |
BACKGROUND: Respiratory syncytial virus (RSV) causes severe respiratory tract infections, which might have a role in the development of airway hyperreactivity. Mast cells are important effector cells in allergy, with sentinel cell roles in host defense. However, the role of mast cells in response to RSV infection is unknown. OBJECTIVE: Human mast cell responses to RSV were investigated with a view to better understanding the role of mast cells in RSV-induced disease. METHODS: Human cord blood-derived mast cells and the HMC-1 mast cell line were exposed to RSV or UV-inactivated RSV. Viral gene and protein expression were evaluated by using PCR and flow cytometry. The expression of interferon-stimulated genes and selected mediators were evaluated by using quantitative PCR and ELISA. RESULTS: Human mast cells expressed multiple RSV genes after exposure to RSV, and a small percentage of mast cells supported RSV antigen protein expression. RSV induced mast cells to upregulate production of chemokines, including CCL4, CCL5, and CXCL10, as well as type I interferons, and interferon-stimulated gene expression. However, production of the granulocyte chemoattractants CXCL8 and CCL11 was not induced. Antibody blockade of the type I interferon receptor on human cord blood-derived mast cells reduced the RSV-mediated induction of CXCL10 and CCL4 but not CCL5. Leukotriene C4 production by mast cells was not enhanced by exposure to RSV. CONCLUSION: Despite low levels of infection, human mast cells produce multiple chemokines in response to RSV through mechanisms that include responses to type I interferons. Such mast cell responses might enhance effector cell recruitment during RSV-induced disease. |
