Please use this identifier to cite or link to this item:http://hdl.handle.net/20.500.12105/9086
Urokinase receptor-deficient mice mount an innate immune response to and clarify respiratory viruses as efficiently as wild-type mice
The plasminogen activator receptor (uPAR) is required for lung infiltration by innate immune cells in respiratory bacterial infections. In order to verify if this held true for respiratory viruses, wild type (WT) and uPAR knockout (uPAR(-/-)) mice were inoculated intranasally with the human respiratory syncytial virus (HRSV) and the influenza A virus. At several days post-infection (dpi), viral titers in the lungs were determined while cell infiltrates in the bronchoalveolar lavage (BAL) were analyzed by flow cytometry. In the case of influenza A, body weight loss and mortality were also monitored. Only minor differences were observed between infected WT and uPAR(-/-) mice, primarily in influenza virus replication and pathology. These results indicate that uPAR does not play a major role in limiting virus replication or in orchestrating the innate immune response against HRSV or influenza infections in mice. This suggests that there are fundamental differences in the immune control of the viral infections studied here and those caused by bacteria.
Influenza A virus | Innate immune response | Respiratory syncytial virus | Urokinase plasminogen activator receptor (uPAR)
Animals | Female | Humans | Immunity, Innate | Influenza A virus | Lung | Male | Mice | Mice, Inbred C57BL | Mice, Knockout | Receptors, Urokinase Plasminogen Activator | Respiratory Syncytial Virus, Human | Respiratory Tract Infections | Survival Analysis | Urokinase-Type Plasminogen Activator | Viral Load | Virus Replication
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