Staphylococcus aureus is the predominant cause of skin and soft tissue infections in humans and with the emergence of methicillin-resistant strains, has prompted the need for alternatives to antibiotics through a better understanding of host immune responses. IL-17-mediated immunity is crucial for host defense against S. aureus skin infections, but the immune cells involved are not entirely defined. Recently, eosinophils were identified to produce IL-17 during fungal infections. However, the role of eosinophils in IL-17-mediated immunity against S. aureus skin infections is unexplored. To investigate the role of eosinophils against S. aureus skin infections, wildtype (wt) and eosinophil-deficient mice were epicutaneously exposed to a bioluminescent strain of S. aureus and bacterial burden monitored over time. Eosinophil-deficient mice had increased bacterial burden compared to wt mice, suggesting that eosinophils contributed to host defense against S. aureus. Next, we used an IL-17A-tdTomato x IL-17F-GFP dual reporter mouse with flow cytometry to determine whether eosinophils produced IL-17A or IL-17F during S. aureus infection. Interestingly, ∼50% of IL-17A-producing cells in the S. aureus-exposed skin were eosinophils, whereas eosinophils did not produce IL-17F. To test whether eosinophil-derived IL-17 protects against S. aureus skin infections, eosinophils were adoptively transferred into IL-17A/F-deficient mice treated with neutralizing mAb against IL-17A+F or an isotype control. Indeed, eosinophils restored the host defense defect in IL-17A/F-deficient mice, but not in the presence of IL-17A+F mAbs, indicating that eosinophil-derived IL-17 promoted host defense. Taken together, we uncovered a novel mechanism whereby eosinophil-derived IL-17 protects against S. aureus skin infections, which has implications in the development of immune-based therapies against S. aureus and potentially other skin infections.