Human parainfluenza virus type 2 (HPIV2) induced host ADAM8 expression in human salivary adenocarcinoma cell line (HSY) during cell fusion
1 Department of Medicine/invärtes medicin, Helsinki University Central Hospital, PO Box 700, FIN-00029 HUS, Helsinki, Finland
2 Department of Virology, Haartman Institute, PL 21 (Haartmaninkatu 3), FIN-00014 University of Helsinki and Helsinki University Hospital Laboratory Division, Helsinki, Finland
3 Department of Orthopedics and Traumatology, Helsinki University Central Hospital, PL 22 (Topeliuksenkatu 5), Helsinki, Finland
4 Department of Medicine/invärtes medicin, Helsinki University Central Hospital, PO Box 700 (Haartamaninkatu 8), FIN-00029 HUS, ORTON Orthopedic Hospital of the ORTON Foundation, Helsinki, Finland; and COXA Hospital for Joint Replacement, Tampere, Finland
Citation and License
BMC Microbiology 2009, 9:55 doi:10.1186/1471-2180-9-55Published: 16 March 2009
The aim of the study was to investigate expression of ADAMs (A Disintegrin and A Metalloproteinase) of host cell origin during cell-cell fusion induced by human parainfluenza virus type 2 (HPIV2).
Induction of host cell ADAM9 was observed in GMK cells, but the applicability of this model was restricted by lack of cross-reactivity of the anti-human ADAM8 antibodies with the corresponding green monkey antigens. HSG cells were not susceptible to HPIV2 virus infection. In contrast, in human parotid gland HSY cells, a natural host cell for paramyxoviruses, HPIV2 induced ADAM8 expression. ADAM8 staining increased dramatically over time from 7.9 ± 3% at zero hours to 99.2 ± 0.8% at 72 hours (p = 0.0001). Without HPIV2 the corresponding percentages were only 7.7% and 8.8%. Moreover, ADAM8 positive cells formed bi- (16.2%) and multinuclear cells (3.5%) on day one and the corresponding percentages on day three were 15.6% for binuclear and 57.2% for multinuclear cells.
ADAM8, well recognized for participation in cell-to-cell fusion especially in osteoclast formation, is up-regulated upon formation of multinuclear giant cells after HPIV2 induction in HSY cells. The virus-HSY cell system provides a novel experimental model for study of the molecular mechanism of cell fusion events.