Asthmatic Bronchial Epithelium Is More Susceptible to Oxidant-Induced Apoptosis
Autor: | Audrey Richter, Ratko Djukanovic, Fabio Bucchieri, Peter H. Howarth, Donna E. Davies, Susan J. Wilson, Jon Ward, James L. Lordan, Sarah M. Puddicombe, Diane Buchanan, Giovanni Zummo, Stephen T. Holgate |
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Přispěvatelé: | Bucchieri, F., Puddicombe, S., Lordan, J., Richter, A., Buchanan, D., Wilson, S., Ward, J., Zummo, G., Howarth, P., Djukanović, R., Holgate, S., Davies, D. |
Rok vydání: | 2002 |
Předmět: |
Adult
Male Pulmonary and Respiratory Medicine Pathology medicine.medical_specialty Cell Biology Molecular Biology Biopsy Clinical Biochemistry Cell Apoptosis Bronchi Inflammation Respiratory Mucosa Biology In vivo medicine Humans Cells Cultured Aged Tumor Necrosis Factor-alpha Epithelial Cells Hydrogen Peroxide Middle Aged Flow Cytometry Oxidants Asthma In vitro Staining medicine.anatomical_structure biology.protein Immunohistochemistry Female Poly(ADP-ribose) Polymerases medicine.symptom Antibody |
Zdroj: | Scopus-Elsevier |
ISSN: | 1535-4989 1044-1549 |
Popis: | Abnormal apoptotic mechanisms are associated with disease pathogenesis. Because the asthmatic bronchial epithelium is characteristically damaged with loss of columnar epithelial cells, we postulated that this is due to unscheduled apoptosis. Using an antibody directed toward the caspase cleavage product of poly(ADP-ribose) polymerase, immunohistochemistry applied to endobronchial biopsies showed higher levels of staining in the bronchial epithelium of subjects with asthma as compared with normal control subjects (% epithelial staining [median (range) = 10.5 (1.4-24.5) versus 0.4 (0.0-9.7)]; P < 0.001). Because we were unable to determine whether this difference was due to ongoing inflammation in vivo, cultures of normal and asthmatic bronchial epithelial cells were used to study apoptosis in vitro. In complete growth medium, these cells showed no difference in their rate of proliferation or viability. However, cells from subjects with asthma were more susceptible to the apoptotic effects of H2O2 than cells from normal control subjects (% apoptotic cells = 32.2 [8.8-54.9] versus 14.3 [6.4-24.7]; P < 0.05), even though both were similarly affected by treatment with actinomycin D. These data indicate that the susceptibility of asthmatic bronchial epithelium to oxidants is greater than normal. This susceptibility may contribute to the rising trends in asthma associated with air pollution and diets low in antioxidants. |
Databáze: | OpenAIRE |
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