Distribution of Mast Cells and Eosinophils in Nasal Polyps from Atopic and Nonatopic Subjects: A Morphometric Study

Abstract

The pathogenetic mechanism of nasal polyps remains unknown, although polyps seem to be an expression of chronic nasal inflammation of both allergic and nonallergic origin. The goal of our study was to compare the distribution mast cells and eosinophils (cells traditionally associated with allergic inflammation) in nasal polyps from well defined atopic and nonatopic patients, using advanced morphometric analysis system. Nasal polyps were removed during routine nasal polypectomy performed in 17 atopic and 19 nonatopic patients. Parrafin sections of nasal polyps were stained with haematoxilin/eosin, chromotrope R2 or toluidine blue, and light microscopy, assisted with computerized picture analysis system, was used to count the number of cells in the superficial and stromal layer of the mucosa. Regardless of the presence or absence of atopy, eosinophils were predominant cells in the polyps, and both eosinophils and mast cells were more abundant in the superficial layer than in the stromal layer of the mucosa. The density of eosinophils in both layers and mast cells in the stromal layer was similar in atopic and nonatopic patients. Only the density of mast cells in the superficial layer of the mucosa was slightly higher (p < 0.005 in atopic compared to nonatopic patients). In both groups of patients a significant correlation between the number of mast cells and eosinophils in the superficial layer of the polyp mucosa was found (r = 0.84; p < 0.001). Our study demonstrates that eosinophils and mast cells are abundant in nasal polyps from both atopic and nonatopic patients and that mast cells seem to be more superficially distributed in atopic compared to nonatopic patients.

Clinicopathological study of nasal polyps with special reference to mast cells in inflammatory polyps

“…Non-neoplastic lesions were classified as inflammatory and allergic polyp depending upon the predominance of eosinophils. In a study conducted by Mysorekar 10 n 20,000 cells/cumm 6,000 cells/cumm Pawliczak et al 11 17 Predominantly in superficial layer of mucosa Present study 91 97.8% (0-5/10 high power field [hpf]) 26% (11-20/10 hpf) et al, 5 89 non-neoplastic nasal polyps were studied, out of which 72 were inflammatory and 18 were allergic polyps. In a 10-year study of 344 cases, Dasgupta et al 3 found 214 neoplastic lesions, out of which 181 were benign and 33 were malignant lesions.…”

“…A few more authors such as Ruhno et al 9 and Otsuka et al 10 have shown that epithelial mast cells in nasal polyps are equally elevated in non-allergic and allergic patients (Table 6). 5,10,11 In another study conducted by Takabayashi, 12 a profound elevation of mast cells was detected within the epithelium and glands of nasal polyps in patients with chronic rhinosinusitis, suggesting that these cells have distinct phenotypes that vary by tissue location. In a study conducted by Kitapci et al, 13 the authors opined that mast cells and eosinophils may have a role in the inflammatory processes, leading to nasal polyposis formation.…”

Spatial expression of two anti‐inflammatory mediators, annexin 1 and galectin‐1, in nasal polyposis

“…see [22]). Migrated eosinophils might contribute to NP aetiology by producing IL-5 and RANTES, cytokines responsible for the tissue-driven inflammatory response [4,23]. In addition, mast cell-derived pro-inflammatory mediators (e.g.…”

“…To detect ANXA1 and Gal-1, tissue samples and human eosinophils were prepared for electron microscopy by standard methods and in sequence a post-embedding immunogold labelling double reaction was performed. Ultrathin sections were incubated: (1) phosphate-buffered solution (PBS) containing 1% egg albumin (PBEA); (2) PBS containing 5% egg albumin (PBEA) for 30 min; (3) the sheep polyclonal antibody raised the N-terminal peptide of human ANXA1 [23] (1 : 200) and the polyclonal rabbit anti-Gal-1 (1 : 300) for 2 h; (4) normal sheep serum and normal rabbit serum, respectively, were used as control; (5) after washes in PBEA, in order to detect ANXA1, a donkey anti-sheep IgG antibody (1 : 50 in PBEA) conjugated to 20 nm colloidal gold (British Biocell, Cardiff, UK) was added, and to detect Gal-1, a goat anti-rabbit IgG antibody (1 : 50 in PBEA) conjugated to 10 nm colloidal gold (British Biocell) was added; and (6) after 1 h, sections were washed in PBEA, and then in distilled water. Ultrathin sections were stained with uranyl acetate and lead citrate before examination on a ZEISS LEO 906 electron microscope.…”

Polipose nasal: caracterização da infiltração dos eosinófilos, mastócitos, miofibroblastos e células TGF-beta positivas em indivíduos com e sem asma

“…Na PN os mastócitos pela micro localização na profundeza do estroma ( Pawliczak et al 1997, Finotto et al 1994, Kawabori et al 1992, Drake-Lee e Price 1997, Sasaki 1986) vão de forma direta, induzir a inflamação eosinofílica através da liberação de vários mediadores inflamatórios (Pawankar 2003, Di Lorenzo et al 2001, ou indiretamente, através da ativação de células estruturais (fibroblastos e miofibroblastos) contribuindo para a formação e progressão dos pólipos nasais.…”