J Asthma Allergy Clin Immunol.
1998 Sep;18(3):441-450.
Evidence for neutrophil activation in induced sputum from patients with
TDI - induced occupational asthma
Abstract
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BACKGROUND: Toluene diisocyanate (TDI) is the most prevalent agent to cause occupational
asthma (OA) in Korea. The pathogenic mechanism of TDI-induced OA is still unclear.
Involvement of both immunological and non-immunologicaI mechanisms have been suggested.
OBJECTIVE
To evaluate a possible role of neutrophil in the development of TDI-asthma.
OBJECT AND METHOD: Myeloperoxidase (MPO) as a neutrophil activation marker in both serum
and induced sputum, and IL-8 in induced sputum were measured. Induced sputa and sera were
collected from 15 TDI-induced OA patients (classified to group I) during
TDI- bronchoprovocation test and were compared with those from 11 asthmatic subjects with
negative TDI-bronchoprovocation test (group II). MPO levels were measured by radioimmunoassay,
IL-8 levels, by enzyme linked immunosorbent assay and albumin levels, by nephelometry.
Sputum MPO and IL-8 levels were presented as a ratio to albumin.
RESULT: Serum MPO level tended to decrease during the TDI-bronchoprovocation test in two
groups, but no statistical significance was reached (p>0.05). However, the ratios of
MPO (the ratio of MPO level measured at 30 min to MPO level at baseline, and the ratio MPO
level measured at 360 min to MPO baseline) in group I were significantly lower than
group II (p=0.004, p=0.03 respectively). The IL-8/albumin and MPO/albumin levels in induced
sputum from group I were significantly increased after the TDI-bronchprovocation test in
comparison to the baseline value which was obtained before the bronchoprovocation test
(p=0.0l, p=0.02 respectively). There was a significant correlation between the percent
increase of IL-8/albumin and the MPO/albumin in induced sputum (r=0.89, p<0.05).
CONCLUSION
These findings suggest a possible involvement of neutrophil in the development
of bronchoconstiction after the TDI exposure, and IL-8 might contribute to neutrophil
recruitment to airway mucosa. Further investigation will be needed to investigate mechanism
of neutrophil activation in the pathogenesis af TDI-induced OA.