Abstract
Pathogenesis of nasal polyposis is incompletely understood. This study investigates the role of inflammatory cells, adhesion molecules, intermediate filaments and chemokine receptors in development of nasal polyposis. Totally, 35 patients were enrolled (Group 1, 10 patients with Samter syndrome; Group 2, 10 patients with diffuse polyposis without signs of Samter syndrome; Group 3, 5 patients with solitary nasal polyps; Group 4, 10 controls). Expression of CD105, CD106, CD62E, CD4, CD8, CXCR4, CD147, CD90, CD104, BF45, vimentin, pancytokeratin and MSA were determined. Expression of CD4, CD8 and CD106 were similar between groups. Ratio of patients expressing CD4 in Group 1, Group 2 and Group 3 were higher than controls. Ratio of patients expressing CD8 antigen were significantly higher in all 3 groups than control group. Expression of CD147 in Group 3 and Group 4 was significantly higher than in Group 1 and Group 2. CD98 expression was higher in Group 1, Group 2 and Group 3 than in Group 4. Ratio of patients expressing vimentin in Group 1, Group 2 and Group 3 were significantly higher than in Group 4. Immunostaining for pancytokeratin was positive in all patients.
In conclusion, inflammatory cells, adhesion molecules, intermediate filaments and chemokine receptors may play a role in pathogenesis of nasal polyps.
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