We have investigated changes of nasal metachromatic cell number, nasal symptoms and nasal provocation at the third and sixth month during allergen immunotherapy. Twenty-five subjects with perennial allergic rhinitis (house dust (23), Alternaria (2) were divided into two groups: an immunotherapy-treated group (n = 14) and a control group (n = 11). At the first visit nasal symptom scores, nasal provocation reactions and the number of metachromatic cells in nasal mucosal epithelial scrapings were not significantly different between groups. At the third and sixth month after immunotherapy nasal symptom scores, nasal provocation and the metachromatic cells in epithelial scrapings were significantly reduced (P less than 0.05) compared with the pretreatment values in the immunotherapy group, but unchanged in the control group. These results suggest that the reduction in metachromatic cell number at the nasal mucosal surface may be one of the mechanisms which could explain the improvement of nasal allergic symptoms by immunotherapy.

We have previously reported highly potent basophil/mast cell (BMC) and basophil/eosinophil (Eo) colony-stimulating activities (CSA) in conditioned medium derived from cultured human nasal polyp epithelial scrapings (NP-CM). We now have examined the involvement of peripheral blood T-cells in the NP-CM stimulation of colony-forming units (cfu) from the blood of atopic and nonatopic subjects. Because the number of BMC- and Eo-cfu was significantly higher in cultures of peripheral blood from subjects with out-of-season ragweed allergic rhinitis than from control subjects (23.8 +/- 4.1 versus 9.0 +/- 2.4, p less than 0.01), we asked whether the observed colony stimulation could be a T-cell-dependent effect. Indeed, peripheral blood target cells consisting of a reconstituted mixture of T-cells and T-cell-depleted peripheral blood mononuclear cells (non-T-cells) yielded a significantly higher number of colonies in the presence of NP-CM than the non-T-cells alone. NP-CM did not stimulate colony formation by isolated T-cells. These observations point to interactions among nasal epithelial growth and differentiation factors, blood-borne progenitors and T-cells in the local accumulation of basophils, mast cells, and eosinophils in nasal polyps.

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The distribution and abundance of mast cells in nasal polyps, the maxillary sinus mucosa of patients with sinusitis and the turbinate mucosa of allergic rhinitis was microscopically examined using different methods of fixation. In the epithelium of the surface and the ducts of nasal polyps (n = 8), the mean number of mast cells was over 20,000 per mm3 using Mota's fixation and the increase was correlated with the epithelial thickness (P<0.05). On the other hand those of the maxillary sinus mucosa (n = 6) and the nasal turbinate mucosa (n = 7) were less than 6,000 per mm3. In the subepithelial layer or areas deeper than the area with the glands, however, mast cell counts were less than 3,200 per mm3 in all diseases. More than 70–90 per cent of all mast cells in the epithelium of the mucosal surface and the ducts of the polyp, the maxillary sinus mucosa and nasal turbinates were formalin sensitive. Most of the mast cells in the subepithelial and deeper areas were formalin resistant in all diseases.These results suggest that conditions for mast cell growth differ between polyps and the other diseases, and that the conditions which affect mast cells may contribute to polyp development.