Proteinase-Activated Receptor-2 Agonist Activates Anti-Influenza Mechanisms and Modulates IFNγ-Induced Antiviral Pathways in Human Neutrophils
Figure 1
IAV replication in neutrophils was restricted by PAR2 activation and IFNγ. (a) Replication of IAV in neutrophils was determined by detection of NS-1 mRNA levels at different time points after infection. At 4 hrs, a significant induction of NS-1 mRNA expression was revealed. In noninfected neutrophils NS-1 mRNA was not detectable. (b) IAV-infected neutrophils were treated with agonists as indicated for 20 hrs. Analysis of IAV titers showed a significant reduction in PAR2 agonist and PAR2 agonist/IFNγ treated neutrophils. (c) In cells that were primed with agonists for 2 hrs, infected with IAV for 30 min, and rechallenged with agonists for 20 hrs, both PAR2 agonist and IFNγ decreased viral replication. Moreover, combining PAR2 agonist and IFNγ further reduced IAV titers as compared to both agonists alone. For student’s t-test: #,*; **; ***. The symbol * marks the significance as compared to control and the symbol # as compared to IFNγ sample.
