Proteinase-Activated Receptor-2 Agonist Activates Anti-Influenza Mechanisms and Modulates IFNγ-Induced Antiviral Pathways in Human Neutrophils

Figure 3

Influenza titers were controlled through extracellular MPO and on transcriptional level through PAR₂. (a, b) DF from stimulated neutrophils was supplemented with H₂O₂, and the virucidal activity was determined. DF from PAR₂ agonist treated neutrophils disrupted IAV. (c) Application of a MPO inhibitor enhanced viral titers. Interestingly, despite MPO inhibition, PAR₂ activation reduced viral replication in neutrophils. (d) Analysis of viral gene replication displayed reduced NS-1 mRNA expression in PAR₂ agonist stimulated neutrophils. IFNγ had no effect on viral replication. For student’s t-test: ^#,*𝑃<0.05; **𝑃<0.01; ***𝑃<0.005. The symbol * marks the significance as compared to control and the symbol # as compared to IFNγ sample.