Objective To explore the role of interleukin-17A (IL-17A) in the pathogenesis of chronic rhinosinusitis (CRS). Methods Nasal polyp specimens were obtained from 38 patients suffering from CRS with nasal polyps (CRSwNP), uncinate process tissues from 15 patients suffering from CRS without nasal polyps (CRSsNP), and normal mucosal tissues from 17 healthy control subjects. Enzyme-linked immunosorbent assay was used to detect the levels of IL-17A, neutrophil-associated chemokines (CXCL1, CXCL2, CXCL8) and tissue remodelling-associated factors (MMP-2, MMP-9, TIMP-1). The localization of IL-17A receptor was detected by immunofluorescence. After stimulation of dispersed nasal polyps cells (DNPCs) with different concentrations of IL-17A, mRNA levels of MMP-2, MMP-9, TIMP-1, CXCL1, CXCL2 and CXCL8 were measured by real-time fluorescence quantitative polymerase chain reaction. Results Compared with the control group, the expression levels of IL-17A, CXCL1, CXCL2, CXCL8, and MMP-9 were elevated in both the CRSwNP and CRSsNP groups, and were more significant in the CRSwNP group (P<0.05). Immunofluorescence revealed that IL-17A receptor was expressed on neutrophils in nasal polyps. The releases of CXCL1, CXCL2, CXCL8, and MMP-9 increased in DNPCs in response to IL-17A stimulation (P<0.05). Conclusions There are significant IL-17A high expression, neutrophil infiltration and tissue remodeling in CRS, especially CRSwNP. IL-17A can stimulate the releases of chemokines CXCL1, CXCL2, and CXCL8 to cause neutrophil infiltration, as well as the production of MMP-9 to promote tissue remodeling in inflammatory regions.