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Proteinase-activated receptor-2 (PAR 2 ) is expressed by human leukocytes and participates in the development of inflammatory diseases. Recent studies demonstrated an ability of PAR 2  agonist to enhance IFN  γ  -induced antiviral responses of human leukocytes. However, the precise cellular antiviral defense mechanisms triggered in leukocytes after stimulation with IFN  γ   and/or PAR 2  agonist remain elusive. Therefore, we aimed to identify neutrophil defense mechanisms involved in antiviral resistance. Here we demonstrated that PAR 2  agonist enhanced IFN  γ  -related reduction of influenza A virus (IAV) replication in human neutrophils. PAR 2 -mediated decrease in IAV replication was associated with reduced NS-1 transcription. Moreover, PAR 2 -dependent neutrophil activation resulted in enhanced myeloperoxidase degranulation and extracellular myeloperoxidase disrupted IAV. The production of ROS was elevated in response to PAR 2  activation. Interestingly, IFN  γ   did not influence both effects: PAR 2  agonist-triggered myeloperoxidase (MPO) release and reactive oxygen species (ROS) production, which are known to limit IAV infections. In contrast, orthomyxovirus resistance gene A (MxA) protein expression was synergistically elevated through PAR 2  agonist and IFN  γ   in neutrophils. Altogether, these findings emphasize two PAR 2 -controlled antiviral mechanisms that are independent of or modulated by IFN  γ  .

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