Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 1996
Intranasal challenge with aspirin induces cell influx and activation of eosinophils and mast cells in nasal secretions of ASA-sensitive patients.
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Kowalski M L, Grzegorczyk J, Wojciechowska B, Poniatowska M
Аннотация
BACKGROUND: Although the mechanism of aspirin-sensitivity seems to be related to inhibition of cyclo-oxygenase by aspirin (ASA), the chain of biochemical events leading to the ASA-induced adverse reaction is not clear, and the contribution of particular mediators and inflammatory cells has not been elucidated.
OBJECTIVES: To investigate the involvement of secretory, vascular and cellular mechanisms in the pathophysiology of nasal reactions to aspirin.
METHODS: Six patients with ASA-sensitive asthma/rhinosinusitis and seven ASA-tolerant patients were challenged intranasaly with saline and lysine-acetylsalicylic acid (Lys-ASA) 12 mg, on separate occasions. Nasal lavages were obtained before, and then every 15 min after challenges, and analysed for biochemical and cellular composition.
RESULTS: Lys-ASA challenge caused rhinorrhoea, sneezing and nasal congestion with parallel increases in total protein and albumin concentration, albumin % and lysozyme activity in the nasal secretions of ASA-sensitive patients. Concomitant with clinical symptoms, an influx of leucocytes into nasal secretions occurred with significant enrichment in eosinophils (mean prechallenge: 24 +/- 12%, postsaline 27 +/- 9%, postLys-ASA 51 +/- 10%; P < 0.03). The influx of eosinophils into nasal secretions was associated with a remarkable increase in Eosinophil Cationic Protein (ECP) immunoreactivity in five of six patients (mean 9.3 +/- 3.8 micrograms/L and 140.9 +/- 45.8 micrograms/mL before and after Lys-ASA, respectively). At the peak of ASA-induced symptoms an increase in the tryptase level was also observed in five of six patients (mean pre-challenge: 2 +/- 0.1 U/L; postLys-ASA 16 +/- 5 U/L; P < 0.01) suggesting activation of mucosal mast cells. In ASA-tolerant patients Lys-ASA did not induce significant symptoms or changes in the biochemical and cellular composition of nasal secretions.
CONCLUSION: The results show that the ASA-induced nasal adverse reaction involves changes in vascular permeability and serous cell secretion. Both activated eosinophils and mast cells may contribute to the pathophysiology of the ASA-induced reaction in the nasal mucosa.
OBJECTIVES: To investigate the involvement of secretory, vascular and cellular mechanisms in the pathophysiology of nasal reactions to aspirin.
METHODS: Six patients with ASA-sensitive asthma/rhinosinusitis and seven ASA-tolerant patients were challenged intranasaly with saline and lysine-acetylsalicylic acid (Lys-ASA) 12 mg, on separate occasions. Nasal lavages were obtained before, and then every 15 min after challenges, and analysed for biochemical and cellular composition.
RESULTS: Lys-ASA challenge caused rhinorrhoea, sneezing and nasal congestion with parallel increases in total protein and albumin concentration, albumin % and lysozyme activity in the nasal secretions of ASA-sensitive patients. Concomitant with clinical symptoms, an influx of leucocytes into nasal secretions occurred with significant enrichment in eosinophils (mean prechallenge: 24 +/- 12%, postsaline 27 +/- 9%, postLys-ASA 51 +/- 10%; P < 0.03). The influx of eosinophils into nasal secretions was associated with a remarkable increase in Eosinophil Cationic Protein (ECP) immunoreactivity in five of six patients (mean 9.3 +/- 3.8 micrograms/L and 140.9 +/- 45.8 micrograms/mL before and after Lys-ASA, respectively). At the peak of ASA-induced symptoms an increase in the tryptase level was also observed in five of six patients (mean pre-challenge: 2 +/- 0.1 U/L; postLys-ASA 16 +/- 5 U/L; P < 0.01) suggesting activation of mucosal mast cells. In ASA-tolerant patients Lys-ASA did not induce significant symptoms or changes in the biochemical and cellular composition of nasal secretions.
CONCLUSION: The results show that the ASA-induced nasal adverse reaction involves changes in vascular permeability and serous cell secretion. Both activated eosinophils and mast cells may contribute to the pathophysiology of the ASA-induced reaction in the nasal mucosa.