Excessive oxidative stress is associated with a deficiency to control pathogenic microbes that can colonise the airways. Streptococcus pneumonia (Spn) is particularly resistant to oxidant-dependent killing mechanisms and infection can be life threatening for immunocompromised people, children under the age of 2 and elderly sufferers of chronic lung diseases such as Chronic Obstructive Pulmonary Disease (COPD). We aimed to elucidate the impact of excessive oxidative stress on innate immune pathways important for the clearance of Spn. A mouse model of high oxidative stress, extracellular-superoxide dismutase 3 (SOD3) deficient mice were used to investigate the mechanism by which oxidative stress compromises pneumococcal clearance. The recruitment of innate immune subsets and expression of their effector molecules were assessed at day 2, and pneumococcal load in the airways was assessed at day 7. At day 2, SOD3KO mice recruited significantly less neutrophils (SOD3KO: 53,252.27±11,908 vs WT: 341,935.95±106,166.30 cells, p<0.05) into the airways as a consequence of a failure to expand IL-17A+ γδ T cells which were proportionally significantly reduced (0.15%±0.017 WT vs 0.08%±0.016 SOD3KO, p<0.05). The lung mucosa of SOD3-deficient mice also had a significant reduction in IL-23 and IL-1β. Since inflammatory macrophages are a major source of these cytokines, CD11b and CD11c were used to track monocytes/macrophage populations, where SOD3-deficiency failed to recruit sufficient numbers of monocytes in response to the bacteria (5,844.69±3,710.37 cells). In contrast, WT mice robustly recruited monocytes (96,661.96±40,595.63 cells) in response to increased production of CCL2, which was significantly reduced in SOD3 deficient mice (SOD3KO: 1,018.76±366.79pg/ml vs WT:2,744.04±532.77pg/ml, p<0.05). As a consequence, significantly higher pneumococcal load (2 log increase, p<0.05) was observed in SOD3-deficient mice at day 7. Overall, this study demonstrated that excessive oxidative stress fails to initiate the IL-17A+ γδ T cell response and the subsequent inflammatory neutrophil/monocyte recruitment required to efficiently eradicate Spn.