Background: Nasal polyp (NP) is a common and frequently occurring disease in otorhinolaryngology head and neck surgery, the pathogenesis of which remains unclear. Differentially expressed genes of mucosal tissues from NP, allergic rhinitis (AR), and normal nasal cavities were screened out by oligonucleotide chip technique and verified by real-time polymerase chain reaction (PCR) and immunohistochemical staining.
Objective: To study gene expression profiles of nasal polyps associated with AR and explore the pathogenic mechanisms of NP at the level of molecular biology.
Methods: Using oligonucleotide chip technique HG-U133A2.0 (Affymetrix, Santa Clara, CA) containing 14500 human full-length genes, gene expression profiles of NP tissues from 6 patients with AR-associated NP, mucosal tissues from the inferior nasal concha of 6 AR patients, and mucosal tissues from the inferior nasal concha of 6 patients with normal nasal cavities were assayed, and differentially expressed genes were analyzed, from which 2 genes (CCL20 and IL-8) that were most up-regulated and 2 genes (RGS1 and GPK4) that were most down-regulated were chosen and verified by real-time PCR. CCL20 protein expression in the NP tissues and normal nasal mucosal tissues of the inferior nasal concha was detected by immunohistochemical staining.
Results: Several hundred differentially expressed genes were screened out by gene chip technique, the functions of which involved inflammatory reaction, immune response, immunoregulation, and signal transduction. Paired comparison of the 3 groups showed the existence of CCL20 up-regulation by more than 2-fold. This result was consistent with that of fluorescent quantitative PCR for differentially expressed genes CCL20, IL-8, RGS1, and GPK4. Immunohistochemical staining showed strong positive expression of CCL20 protein in epithelial cells and submucosal glanular cells of NP tissues and weak positive expression in those of mucosal tissues of the normal inferior nasal concha. The difference was statistically significant (P < .05).
Conclusion: There were differences in gene expression profiles of AR associated NP, and these differentially expressed genes provide new cues for the study of pathogenesis of NP. Up-regulation of chemokine CCL20 may be an important factor of NP occurrence, and down-regulation of signal transduction genes may also be involved in the development of NP.