Evidence for neutrophil activation in induced sputum from patients with TDI - induced occupational asthma

Abstract

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. Material 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. Results: 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.