Neutrophil activation following TDI bronchial challenges to the airway secretion from subjects with TDI-induced asthma
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 bronchoconstriction after TDI inhalation. Objectives To further understand the role...
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Published in | Clinical and experimental allergy Vol. 29; no. 10; pp. 1395 - 1401 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford BSL
Blackwell Science Ltd
01.10.1999
Blackwell Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
ISSN | 0954-7894 1365-2222 |
DOI | 10.1046/j.1365-2222.1999.00682.x |
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Summary: | 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 bronchoconstriction after TDI inhalation.
Objectives
To further understand the role of neutrophils in the pathogenesis 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 symptoms and worked in the same workplace, but showed negative bronchial challenges were enrolled as controls (group II). Serum neutrophil chemotactic activity during TDI bronchial challenge test was measured by the Boyden chamber 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 changes were found in group II subjects (P > 0.05). MPO and IL‐8 were abundantly 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 contribute to bronchoconstriction induced by TDI which may be associated with IL‐8 release. |
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Bibliography: | ArticleID:CEA682 ark:/67375/WNG-FNFMQX4B-D istex:0C17D0617B5749E48E148419D108A1C0938AA75F ObjectType-Article-1 SourceType-Scholarly Journals-1 content type line 14 ObjectType-Feature-2 content type line 23 |
ISSN: | 0954-7894 1365-2222 |
DOI: | 10.1046/j.1365-2222.1999.00682.x |