Background: We investigated the association among tissue eosinophilia, cellular infiltration, and cytokine mRNA expression in chronic hyperplastic sinusitis (CHS).
Methods: Percutaneous biopsies of the maxillary sinuses and nasal polyps were performed in 12 adult patients (six men and six women) of whom seven were nonallergic and 11 were asthmatic. Tissues were compared with biopsy specimens from the inferior and middle turbinates of normal control subjects.
Results: Histologically, an eosinophil-predominant inflammatory infiltrate was seen in 10 of 12 patients, whereas a mild to moderate neutrophilic infiltrate was seen in 4 of 12 patients. As determined by immunocytochemistry, diseased tissues and normal control tissues differed significantly in terms of the number of activated (EG2+) eosinophils (p = 0.005) but not in terms of CD3+ or CD4+ T lymphocytes, elastase-positive neutrophils or CD68+ macrophages. The number of eosinophils did not correlate with that of any other cell type. By in situ hybridization, CHS tissues showed significantly higher numbers of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-3 mRNA-positive cells than normal control tissues (p = 0.002 and 0.0005, respectively) per high-powered field. There was a significant correlation between the number of infiltrating EG2+ eosinophils and cells that expressed mRNA for GM-CSF (r = 0.60, p = 0.041) or IL-3 (r = 0.69, p = 0.013). Furthermore, epithelial cells did not show detectable mRNA expression for GM-CSF or IL-3. No significant correlation was found between IL-5 mRNA expression and infiltrating EG2+ eosinophils in diseased tissues. However, the IL-5 density was significantly higher in the five patients with CHS who had positive allergy skin test results than in the seven patients with negative skin test results (p = 0.017) or in normal control subjects.
Conclusions: Our data support a role for GM-CSF and IL-3 in the eosinophilia characteristic of CHS and show that IL-5 mRNA expression is not a prominent feature of nonallergic inflammation. The cellular sources of GM-CSF and IL-3 in CHS remain to be definitely determined.