Decreased apoptosis and distinct profile of infiltrating cells in the nasal polyps of patients with aspirin hypersensitivity.
BACKGROUND
Patients with aspirin-hypersensitive rhinosinusitis/asthma suffer from a severe form of hyperplastic rhinosinusitis with recurrent polyposis. We aimed to assess the presence of apoptotic cells in nasal polyps from aspirin-hypersensitive (AH) and aspirin-tolerant (AT) patients with rhinosinusitis as related to the characteristics of local inflammation.


METHODS
Nasal polyps obtained from 16 AH patients and 36 AT patients (17 atopic and 19 nonatopic) were stained for eosinophils and metachromatic cells, and in parallel immunocytochemistry was performed to detect CD45RO+, HLA-DR+, CD8+ and CD68+ positive cells. Apoptotic cells were detected by a nick-end labelling technique, TUNEL.


RESULTS
The density of apoptotic cells in AH polyps (5.5 + 1.5 cells/mm2) was significantly lower as compared to both atopic (18.7 + 3.8 cells/mm2; P < 0.02;) and nonatopic (21.3 + 5.2 cells/mm2; P < 0.01) AT polyps. The number of eosinophils, mast cells, and CD45RO+ cells were significantly increased in AH compared to AT polyps (P < 0.001), and the density of HLA-DR+ cells in AH patients was higher than in nonatopic (P < 0.02), but not in atopic AT patients. While in AH patients the duration of rhinosinusitis correlated inversely with the number of apoptotic cells (r = - 0.67; P < 0.04), in contrast, in AT atopic patients the duration of rhinosinusitis showed positive correlation with apoptosis (r = 0.89; P < 0.003).


CONCLUSIONS
We conclude, that decreased apoptosis of inflammatory cells in nasal polyps from ASA-hypersensitive patients, reflects a distinct mechanisms of local inflammation and may be related to persistence and severity of the disease in these patients.
Kowalski
M L
ML
Department of Clinical Immunology and Allergy, Faculty of Medicine, Medical University, Lódz, Poland.
Grzegorczyk
J
J
Pawliczak
R
R
Kornatowski
T
T
Wagrowska-Danilewicz
M
M
Danilewicz
M
M
D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D015703:Antigens, CD / Q000502:physiology; D015214:Antigens, Differentiation, Myelomonocytic / Q000502:physiology; D000954:Antigens, Surface / Q000502:physiology; D017209:Apoptosis / Q000502:physiology*; D001241:Aspirin / Q000009:adverse effects*; D018414:CD8-Positive T-Lymphocytes / Q000502:physiology; D004342:Drug Hypersensitivity / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D004804:Eosinophils / Q000502:physiology; D006684:HLA-DR Antigens / Q000502:physiology; D006801:Humans; D017493:Leukocyte Common Antigens / Q000502:physiology; D008407:Mast Cells / Q000502:physiology; D008875:Middle Aged; D009297:Nasal Mucosa / Q000166:cytology / Q000503:physiopathology; D009298:Nasal Polyps / Q000473:pathology* / Q000503:physiopathology*; D012220:Rhinitis / Q000209:etiology / Q000503:physiopathology; D012852:Sinusitis / Q000209:etiology / Q000503:physiopathology; D013223:Statistics as Topic; D000097382:CD68 Molecule
D000894:Anti-Inflammatory Agents, Non-Steroidal; D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000954:Antigens, Surface; D001241:Aspirin; D006684:HLA-DR Antigens; D017493:Leukocyte Common Antigens; C067980:CD68 antigen, human; D000097382:CD68 Molecule