Relation of epidermal growth factor receptor expression to goblet cell hyperplasia in nasal polyps

Background: Because the epidermal growth factor receptor (EGFR) system regu lates mucin production in airway epithelium, we hypothesized a role for thi s system in mucus hypersecretion that occurs in nasal polyposis. Objective: We examined the relationship between goblet cell hyperplasia, EG FR expression, and inflammatory mediators produced by eosinophils and neutr ophils in nasal polyp tissues, Methods: Nasal polyp tissue samples from 8 patients and nasal turbinate bio psy specimens from 6 normal control subjects were examined for alcian blue/ PAS staining, mucin MUC5AC (MUC5AC), and EGFR immunoreactivity and EGFR gen e expression (in situ hybridization). We also examined the role of eosinoph ils and neutrophils in goblet cell hyperplasia, Results: In control nasal mucosa alcian blue/periodic acid-Schiff- and MUC5 AC-stained areas were 18.40% +/- 1.31% and 21.89% +/- 1.43%, respectively. In polyps the alcian blue/periodic acid-Schiff- and MUC5AC-stained areas we re 51.30% +/- 5.85% and 52.07% +/- 6.58%, which was significantly larger th an that found in control subjects (each comparison, P < .01). Four of 6 con trol specimens expressed EGFR messenger RNA and protein weakly in the epith elium. In polyps 4 of 8 specimens expressed EGFR gene and EGFR protein stro ngly; the EGFR-stained area was greater in hyperplastic than in pseudostrat ified epithelium. TNF-<alpha> immunoreactivity, expressed in eosinophils, w as increased in EGFR-positive polyps compared with EGFR-negative polyps, su ggesting a role for TNF-alpha in EGFR expression. Neutrophils were increase d in the epithelium of EGFR-positive compared with EGFR-negative polyps, su ggesting a role for these cells in mucin expression and in goblet cell degr anulation, Conclusion: These data suggest a role for EGFR cascade in the regulation of goblet cell mucins in nasal polyps. Proof of concept will require clinical studies using selective EGFR inhibitors.