American journal of rhinology & allergy · 2010
Expression of a disintegrin and metalloproteinase 33 protein in nasal polyposis: an immunohistochemical study.
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Erbek Selim S, Erinanc Hilal, Erbek Seyra, Topal Ozgul, Kiyici Halil
Аннотация
BACKGROUND: A disintegrin and metalloproteinase (ADAM)-33 is a member of matrix metalloproteinases. This protein takes a role in angiogenesis and airway remodeling in asthma. Because histopathological findings of airway remodeling in asthma and nasal polyposis (NP) are similar, the aim of this study was to evaluate the ADAM-33 expression in NP.
METHODS: Immunohistochemical staining of specimens of 47 patients with NP and 8 patients with concha bullosa was performed to detect the expression of ADAM-33. Paraffin blocks were used to identify the expression of ADAM-33 polyclonal antibodies. Immunostaining of epithelial cells, stroma, mesenchymal cells of vessels, and inflammatory cells were analyzed by using light microscopy.
RESULTS: Immunopositivity scores in epithelial cells in NP (median, 2; range, 1-3) were significantly higher than those of controls (median, 1.5; range, 1-2; p < 0.001). ADAM-33 staining was increased in the mesenchymal cells of vessels of nasal polyps (median, 2; range, 1-3) compared with control tissues (median, 1.5; range, 1-2; p = 0.006). Although the staining scores of fibroblasts in nasal polyp specimens were also high (median, 3; range 1-3), there was no statistical significance when compared with controls (median 2; range, 1-3; p = 0.228). ADAM-33 immunostaining was not related with the presence of allergies, asthma, and aspirin intolerance (p > 0.05). Moreover, no relationship was found between increased expression of ADAM-33 and the stages of polyp or computerized tomography scores (p > 0.05).
CONCLUSION: This study suggests that the increased expression of ADAM-33 protein may have a role in the pathogenesis of NP.
METHODS: Immunohistochemical staining of specimens of 47 patients with NP and 8 patients with concha bullosa was performed to detect the expression of ADAM-33. Paraffin blocks were used to identify the expression of ADAM-33 polyclonal antibodies. Immunostaining of epithelial cells, stroma, mesenchymal cells of vessels, and inflammatory cells were analyzed by using light microscopy.
RESULTS: Immunopositivity scores in epithelial cells in NP (median, 2; range, 1-3) were significantly higher than those of controls (median, 1.5; range, 1-2; p < 0.001). ADAM-33 staining was increased in the mesenchymal cells of vessels of nasal polyps (median, 2; range, 1-3) compared with control tissues (median, 1.5; range, 1-2; p = 0.006). Although the staining scores of fibroblasts in nasal polyp specimens were also high (median, 3; range 1-3), there was no statistical significance when compared with controls (median 2; range, 1-3; p = 0.228). ADAM-33 immunostaining was not related with the presence of allergies, asthma, and aspirin intolerance (p > 0.05). Moreover, no relationship was found between increased expression of ADAM-33 and the stages of polyp or computerized tomography scores (p > 0.05).
CONCLUSION: This study suggests that the increased expression of ADAM-33 protein may have a role in the pathogenesis of NP.