IMMUNOHISTOCHEMICAL CHARACTERIZATION OF CELLULAR INFILTRATE IN NASAL POLYP FROM ASPIRIN-SENSITIVE ASTHMATIC-PATIENTS

Background: The immunopathologic mechanism of nasal polyp in aspirin-s ensitive asthma remains to be further defined. Objective: To character ize the features of the inflammatory cellular infiltrate in the nasal polyp tissue from aspirin-sensitive asthmatic patients. Methods: We ha ve taken nasal polyp tissue during nasal polyp resection from 13 aspir in-sensitive asthma, 6 allergic, and 12 non-allergic subjects. Immunoh istochemistry was employed to stain and enumerate the individual infla mmatory cell types using monoclonal antibodies against tryptase (AA1) to identify mast cells, against secreted forms of eosinophil cationic protein (EG2), to identify activated eosinophils, against neutrophil e lastase (NE) for neutrophils and against T cell surface markers (CD3) to identify total T cells. Results: There were no significant differen ces in AA1 + cells among three groups (P>.05). EG2 + cells tended to b e higher in ASA-sensitive asthmatic patients than in allergic and non- allergic subjects, but no statistical significance was observed. NE+ c ells were found in most subjects of the three groups and their numbers were significantly higher in allergic subjects than in aspirin-sensit ive asthma (P<.05). Some patients had CD3+ cells with no statistical s ignificance among the three groups. Significant correlation was found in numbers between NE+ cell and AA1 + cell (r=.44, P=.01), and between NE+ cell and EG2+ cell (r=.40, P=.02). Conclusion: These findings sug gested that major effector cells such as mast cells and eosinophils mi ght be placed in the center of the inflammatory response of nasal poly ps, regardless of their association with aspirin sensitivity.