Background: Chronic rhinosinusitis (CRS) comprises heterogeneous eosinophilic (type-2) and neutrophilic (type-1/3) endotypes, yet existing murine models rarely distinguish them or compare their therapeutic responsiveness. Methods: Seven-week-old female C57BL/6N mice received intranasal instillations three times weekly for 4 or 12 weeks with either (1) a clinically relevant airborne allergen cocktail (house dust mite [HDM], Aspergillus fumigatus, Alternaria alternata, and Staphylococcus aureus protease) to induce eosinophilic CRS (ECRS) or (2) an innate stimulus mixture (lipopolysaccharide, β-1,3-glucan, and S. aureus protease) to induce neutrophilic CRS (NCRS). A parallel cohort received weekly dexamethasone administration (2 mg/kg). Endpoints included flow cytometry, enzyme-linked immunosorbent assays, quantitative PCR, histology, and immunofluorescence assays. Results: Four-week allergen exposure produced a pure ECRS phenotype characterized by robust tissue eosinophilia, type-2 cytokines, and marked responsiveness to dexamethasone. Extending allergen delivery to 12 weeks generated mixed CRS with superimposed neutrophilia, upregulation of Il1b/Tgfb1 , mucus hypersecretion, and attenuated steroid efficacy. Innate stimulus treatment yielded a steroid-resistant NCRS phenotype dominated by neutrophils, elevated Ifng/Il17a expression, and minimal type-2 biomarkers. Systemic eotaxin and HDM-specific immunoglobulin E mirrored those found in local eosinophilia, whereas circulating granulocytes remained unchanged across groups. Conclusions: By adjusting the stimulus type and duration, we established tunable murine models that recapitulate pure ECRS, mixed CRS, and steroid-resistant NCRS within a single genetic background. These paired models provide a versatile platform for dissecting endotype-specific mechanisms and evaluating tailored interventions, highlighting the potential importance of early, phenotype-directed CRS therapy.