H S Park1, D H Nahm, K Park, K S Suh, H E Yim. 1. Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea.
Abstract
BACKGROUND: The immunopathologic mechanism of nasal polyp in aspirin-sensitive asthma remains to be further defined. OBJECTIVE: To characterize the features of the inflammatory cellular infiltrate in the nasal polyp tissue from aspirin-sensitive asthmatic patients. METHODS: We have taken nasal polyp tissue during nasal polyp resection from 13 aspirin-sensitive asthma, 6 allergic, and 12 non-allergic subjects. Immunohistochemistry was employed to stain and enumerate the individual inflammatory 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 elastase (NE) for neutrophils and against T cell surface markers (CD3) to identify total T cells. RESULTS: There were no significant differences in AA1 + cells among three groups (P>.05). EG2 + cells tended to be higher in ASA-sensitive asthmatic patients than in allergic and non-allergic subjects, but no statistical significance was observed. NE+ cells were found in most subjects of the three groups and their numbers were significantly higher in allergic subjects than in aspirin-sensitive asthma (P<.05). Some patients had CD3+ cells with no statistical significance 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 suggested that major effector cells such as mast cells and eosinophils might be placed in the center of the inflammatory response of nasal polyps, regardless of their association with aspirin sensitivity.
BACKGROUND: The immunopathologic mechanism of nasal polyp in aspirin-sensitive asthma remains to be further defined. OBJECTIVE: To characterize the features of the inflammatory cellular infiltrate in the nasal polyp tissue from aspirin-sensitive asthmatic patients. METHODS: We have taken nasal polyp tissue during nasal polyp resection from 13 aspirin-sensitive asthma, 6 allergic, and 12 non-allergic subjects. Immunohistochemistry was employed to stain and enumerate the individual inflammatory 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 elastase (NE) for neutrophils and against T cell surface markers (CD3) to identify total T cells. RESULTS: There were no significant differences in AA1 + cells among three groups (P>.05). EG2 + cells tended to be higher in ASA-sensitive asthmatic patients than in allergic and non-allergic subjects, but no statistical significance was observed. NE+ cells were found in most subjects of the three groups and their numbers were significantly higher in allergic subjects than in aspirin-sensitive asthma (P<.05). Some patients had CD3+ cells with no statistical significance 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 suggested that major effector cells such as mast cells and eosinophils might be placed in the center of the inflammatory response of nasal polyps, regardless of their association with aspirin sensitivity.
Authors: Jong Sook Park; An Soo Jang; Sung Woo Park; Young Mok Lee; Soo Taek Uh; Yong Hoon Kim; Ji Yean Cha; Se Min Park; Choon-Sik Park Journal: Allergy Asthma Immunol Res Date: 2009-12-30 Impact factor: 5.764
Authors: Ma Cristina Negrete-Garcia; Carla Yoneli Jiménez-Torres; Noe Alvarado-Vásquez; A Rosalía Montes-Vizuet; J R Velázquez-Rodriguez; M Carmen Jimenez-Martinez; Luis Manuel Teran-Juárez Journal: ScientificWorldJournal Date: 2012-04-30