We have studied the phenotype and activation status of leukocytes in the bronchial mucosa in patients with isocyanate-induced asthma. Fiberoptic bronchial biopsy specimens were obtained from nine subjects with occupational (five toluene- and four methylene diisocyanate-sensitive) asthma, 10 subjects with extrinsic asthma, and 12 nonatopic healthy control subjects. Bronchial biopsy specimens were examined by immunohistology with a panel of monoclonal antibodies and the alkaline phosphatase—antialkaline phosphatase method. There was a significant increase in the number of CD25+ cells (interleukin-2 receptor-bearing cells, presumed “activated” T-lymphocytes; p < 0.01) in isocyanate-induced asthma compared with that of control subjects. There were also significant increases in major basic protein (BMK-13)-positive (p < 0.02) and EG2-positive (p < 0.01) cells that represent total and “activated” eosinophil cationic protein—secreting eosinophils, respectively. In agreement with our previous findings, CD25+ (p < 0.01), BMK-13 (p < 0.03), and EG2+ (p < 0.01) cells were also elevated in extrinsic asthma. No significant differences were observed in the numbers of T-lymphocyte phenotypic markers (CD3, CD4, and CD8) between subjects with asthma (isocyanate-induced and extrinsic) and control subjects. Similarly, no significant differences in immunostaining for neutrophil elastase (neutrophils) or CD68 (macrophages) were observed. The results suggest that isocyanate-induced occupational asthma and atopic (extrinsic) asthma have a similar pattern of inflammatory cell infiltrate. The results support the view that T-lymphocyte activation and eosinophil recruitment may be important in asthma of diverse etiology.

Activated T-lymphocytes and eosinophils in the bronchial mucosa in isocyanate-induced asthma / A. M., Bentley; P., Maestrelli; M., Saetta; Fabbri, Leonardo; D. S., Robinson; B. L., Bradley; P. K., Jeffery; S. R., Durham; A. B., Kay. - In: JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY. - ISSN 0091-6749. - STAMPA. - 89:(1992), pp. 821-829.

Activated T-lymphocytes and eosinophils in the bronchial mucosa in isocyanate-induced asthma.

FABBRI, Leonardo;
1992

Abstract

We have studied the phenotype and activation status of leukocytes in the bronchial mucosa in patients with isocyanate-induced asthma. Fiberoptic bronchial biopsy specimens were obtained from nine subjects with occupational (five toluene- and four methylene diisocyanate-sensitive) asthma, 10 subjects with extrinsic asthma, and 12 nonatopic healthy control subjects. Bronchial biopsy specimens were examined by immunohistology with a panel of monoclonal antibodies and the alkaline phosphatase—antialkaline phosphatase method. There was a significant increase in the number of CD25+ cells (interleukin-2 receptor-bearing cells, presumed “activated” T-lymphocytes; p < 0.01) in isocyanate-induced asthma compared with that of control subjects. There were also significant increases in major basic protein (BMK-13)-positive (p < 0.02) and EG2-positive (p < 0.01) cells that represent total and “activated” eosinophil cationic protein—secreting eosinophils, respectively. In agreement with our previous findings, CD25+ (p < 0.01), BMK-13 (p < 0.03), and EG2+ (p < 0.01) cells were also elevated in extrinsic asthma. No significant differences were observed in the numbers of T-lymphocyte phenotypic markers (CD3, CD4, and CD8) between subjects with asthma (isocyanate-induced and extrinsic) and control subjects. Similarly, no significant differences in immunostaining for neutrophil elastase (neutrophils) or CD68 (macrophages) were observed. The results suggest that isocyanate-induced occupational asthma and atopic (extrinsic) asthma have a similar pattern of inflammatory cell infiltrate. The results support the view that T-lymphocyte activation and eosinophil recruitment may be important in asthma of diverse etiology.
89
821
829
Activated T-lymphocytes and eosinophils in the bronchial mucosa in isocyanate-induced asthma / A. M., Bentley; P., Maestrelli; M., Saetta; Fabbri, Leonardo; D. S., Robinson; B. L., Bradley; P. K., Jeffery; S. R., Durham; A. B., Kay. - In: JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY. - ISSN 0091-6749. - STAMPA. - 89:(1992), pp. 821-829.
A. M., Bentley; P., Maestrelli; M., Saetta; Fabbri, Leonardo; D. S., Robinson; B. L., Bradley; P. K., Jeffery; S. R., Durham; A. B., Kay
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/593789
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