Neutrophil infiltration and release of IL-8 in airway mucosa from subjects with grain dust-induced occupational asthma.
Park, HS; Jung, KS; Hwang, SC; Nahm, DH; Yim, HE
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology, 28(6):724-730, 1998
Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
BACKGROUND: The immuno-pathological mechanism for occupational asthma induced by grain dust (GD) remains to be clarified. There have been few reports suggesting the involvement of neutrophils inducing bronchoconstriction after inhalation of GD.
OBJECTIVE: To further understand the role of neutrophil in the pathogenesis of GD-induced asthma.
MATERIALS AND METHODS: We studied the phenotype of leucocytes of the bronchial mucosa in patients with GD-induced asthma. Bronchial biopsy specimens were obtained by fibreoptic bronchoscopy from six subjects with GD-induced asthma. Six allergic asthma patients sensitive to house dust mite were enrolled as controls. Bronchial biopsy specimens were examined by immunohistochemistry with a panel of monoclonal antibodies to tryptase-containing mast cell (AA1), activated eosinophil (EG2), pan T-lymphocyte (CD3) and neutrophil elastase (NE). Induced sputum was collected before and after the GD-bronchoprovocation test. The IL-8 level in the sputum was measured using ELISA.
RESULTS: There was a significant increase in the number of AA1+ and NE+ cells in bronchial mucosa of GD-induced asthma, compared with those of allergic asthma (P=0.01, P=0.01, respectively). No significant differences were observed in the number of EG2+ and CD3+ cells (P = 0.13, P=0.15, respectively). IL-8 was abundant in the sputum of all GD-induced asthma patients and significantly increased after the bronchial challenges compared with the baseline value (P = 0.03).
CONCLUSION: These findings support the view that neutrophil recruitment together with mast cells may contribute to the bronchoconstriction induced by GD. A possible involvement of IL-8 was suggested.
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