Respiratory viruses such as Influenza A Virus (IAV) and SARS-CoV-2 trigger excessive inflammation, often leading to severe pathology. Neutrophils, key early responders in the immune system, produce reactive oxygen species (ROS) via NADPH oxidase (Nox2), balancing pathogen clearance and immune regulation. Our study explores how neutrophil Nox2-derived ROS curtails inflammatory circuits involving IL-1β and IL-17A, thus promoting effective viral clearance without exacerbating inflammation. We used neutrophil-specific Nox2 knockout mice in an IAV model to demonstrate that Nox2-derived ROS suppress neutrophil-driven IL-1β production, which in turn limits IL-17A-producing γδ T cells. In the absence of Nox2, increased IL-1β production creates a self-amplifying loop with IL-17A, which impairs the antiviral interferon response, heightens lung inflammation, and delays viral clearance. These findings were extended to human neutrophils exposed to virus analogs and SARS-CoV-2, where Nox2-mediated ROS similarly regulated IL-1β and IL-17A signaling. This study reveals a dual role for ROS: while traditionally associated with oxidative damage, Nox2-derived ROS act as immune modulators, balancing inflammatory responses and enhancing pathogen clearance. These insights suggest that therapeutic strategies aimed at modulating ROS levels could improve outcomes in viral infections by enhancing antiviral immunity while preventing inflammatory damage.