Neutrophil activation following TDI bronchial challenges to the airway secretion from subjects with TDI-induced asthma

Citation
Hs. Park et al., Neutrophil activation following TDI bronchial challenges to the airway secretion from subjects with TDI-induced asthma, CLIN EXP AL, 29(10), 1999, pp. 1395-1401
Citations number
31
Categorie Soggetti
Clinical Immunolgy & Infectious Disease",Immunology
Journal title
CLINICAL AND EXPERIMENTAL ALLERGY
ISSN journal
09547894 → ACNP
Volume
29
Issue
10
Year of publication
1999
Pages
1395 - 1401
Database
ISI
SICI code
0954-7894(199910)29:10<1395:NAFTBC>2.0.ZU;2-8
Abstract
Background The immunopathological mechanism for occupational asthma induced by toluene diisocyanate (TDI) remains to be further clarified. There have been few reports suggesting involvement of neutrophils in inducing bronchoc onstriction after TDI inhalation. Objectives To further understand the role of neutrophils in the pathogenesi s of TDI-induced asthma. Materials and methods Eight TDI-induced asthmatic subjects were classified as group I, and five exposed workers who had complained of work-related sym ptoms and worked in the same workplace, but showed negative bronchial chall enges were enrolled as controls (group IT). Serum neutrophil chemotactic ac tivity during TDI bronchial challenge test was measured by the Boyden chamb er method. Induced sputum was collected before and after the TDI bronchial challenge test. The myeloperoxidase (MPO) and interleukin (IL) -8 levels in the sputum were measured using RIA and ELISA. Result Serum neutrophil chemotactic activity significantly increased at 10 min (P = 0.01), then decreased at 60 min (P = 0.02) and remained unchanged for up to 420 min (P = 0.07) in group I subjects, while no significant chan ges were found in group II subjects (P > 0.05). MPO and IL-X were abundantl y present in the sputum of all the TDI-induced asthmatic subjects and they increased significantly at 420 min after the bronchial challenges (P = 0.02 , P = 0.03, respectively), while no significant changes were noted in group II subjects (P > 0.05). Conclusion These findings support the view that activated neutrophils may c ontribute to bronchoconstriction induced by TDI which may be associated wit h IL-8 release.