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Neutrophil chemotactic factor of anaphylaxis (NCF‐A) release in aspirin‐induced asthma
Author(s) -
ORTOLANI C.,
CAPSONI F.,
RESTUCCIA M.,
PASTORELLO E.,
RIBOLDI P. S.,
ZOCCHI M.,
ZANUSSI C.
Publication year - 1984
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.1984.tb02228.x
Subject(s) - bronchoconstriction , medicine , asthma , cromolyn sodium , aspirin , chemotaxis , anaphylaxis , immunology , platelet activating factor , degranulation , allergy , pharmacology , receptor
Summary Neutrophil chemotactic activity (NCA) following oral challenge with aspirin (ASA) was determined in ASA‐intolerant asthmatic subjects, and in ASA‐tolerant asthmatic and normal subjects. There was a statistically significant fall in FEV 1 and a rise in NCA ( P <0.01) following challenge in the ASA‐sensitive subjects compared with that of the ASA‐tolerant subjects and normal controls. No significant difference was observed between the latter two groups. The chemotactic factor identified in this study had a molecular weight greater than 150 000 which is consistent with NCF‐A (neutrophil chemotactic factor of anaphylaxis). The ASA‐induced fall in FEV 1 and rise in NCA was further studied in three of the ASA‐intolerant asthmatic subjects, with and without pretreatment with inhaled sodium cromoglycate. In these subjects, the drug inhibited both the oral ASA‐induced bronchoconstriction and the increase in neutrophil chemotactic activity. These results suggest that ASA‐induced asthma involves mediator release from mast cells, as shown by the increase in NCA following ASA challenge and the protective effect of sodium cromoglycate which is considered to inhibit mast‐cell degranulation.