These findings suggest that S100A9 may be a key mediator that polarizes M1 macrophages by activating neutrophils, facilitating proinflammatory cytokine production, shifting to non-type 2 airway inflammation/remodeling, and progressing to SA; S100A9 may be a potential therapeutic target for suppressing M1-mediated neutrophilic inflammation via the AEC-S100A9-macrophage polarization–neutrophil axis in NA. The gene discussed is S100A9; the disease is inflammation.