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.
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.
The function of nasal polyp mast cells has not been elucidated despite the large number of these cells observed in tissues.We examined these mast cells histochemically, immunohistologically and functionally.Ninety-three percent of collagenase dispersed cells in a nasal polyp were formalin-sensitive.These dispersed cells released histamine in reaction to calcium ionophore A23187 in a dose dependent manner, but not in response to C5a, Compound 48/80 or Substance P. From these results, dispersed mast cells from nasal polyps were considered to be analogous to dispersed mast cells from the human lung and nasal mucosa but not those from human skin.On the other hand, in the reaction with anti-human IgE, dispersed mast cells from a non allergic nasal polyp could not be seen to release histamine. In only 2 of 7 patients, could histamine release in response to Japanese red cedar antigen, from mast cells sensitized passively with the serum of Japanese red cedar pollinosis, seen. Using small tissue samples from polyps, histamine was released by anti-human IgE in allergic patients but not in non allergic patients.Immunohistologically in allergic nasal polyps, some IgE positive mast cells could be seen, whereas in non allergic polyps these cells were absent.These observations suggest that mast cells which had accumulated in nasal polyps both with and without allergy were capable of functional histamine release, whereas in the nasal polyps of allergy patients but not in non-allergic patients these cells are involved in IgE mediated reactions.
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