Background: Apoptosis regulates inflammatory cell survival, and its reduction contributes to the chronicity of an inflammatory process. Apoptosis is controlled by suppressing or inducing genes, such as bcl-2 and p53, respectively. Objective:We sought to assess apoptosis of eosinophils, macrophages, and T lymphocytes in bronchial biopsy specimens from asthmatic subjects and to examine its regulation by evaluating the expression of B-cell lymphoma leukemia-2 (Bcl- 2) and P53 proteins. We also sought to explore the relationships between cell apoptosis and GM-CSF, a cytokine able to increase eosinophil and macrophage survival. Methods: Apoptosis in eosinophils, macrophages, and T lymphocytes was evaluated in bronchial biopsy specimens obtained from 30 asthmatic subjects, 26 subjects with chronic bronchitis, and 15 control subjects by combining the terminal deoxynucleotidyl transferase-mediated dNTP nick end-labeling technique and immunohistochemistry. The expression of P53, Bcl-2, and GM-CSF was studied through immunohistochemistry by using specific mAbs. Results: The number of apoptotic eosinophils and macrophages was lower in subjects with asthma than in those with chronic bronchitis (P < .007 and P < .001, respectively) and inversely correlated with the clinical severity of asthma (P < .001 and P < .002, respectively). Few T lymphocytes were apoptotic in all groups studied. In asthma GM-CSF+ cells correlated with the number of nonapoptotic eosinophils and macrophages (P = .0001) and with the severity of the disease (P < .003). In asthma Bcl-2+ cells were higher than in control subjects and subjects with chronic bronchitis (P < .002 and P < .015, respectively), they outnumbered P53+ cells, and they correlated with the number of T lymphocytes (P < .001) and with the severity of the disease (P < .003). Conclusion: Airway inflammation in asthma is associated with an e nhanced survival of different cell types caused by reduced apoptosis.
Evaluation of apoptosis of eosinophils, macrophages, and T lymphocytes in mucosal biopsy specimens of patients with asthma and chronic bronchitis.
Chiappara G;Siena L;Gagliardo R;Profita M;
1999
Abstract
Background: Apoptosis regulates inflammatory cell survival, and its reduction contributes to the chronicity of an inflammatory process. Apoptosis is controlled by suppressing or inducing genes, such as bcl-2 and p53, respectively. Objective:We sought to assess apoptosis of eosinophils, macrophages, and T lymphocytes in bronchial biopsy specimens from asthmatic subjects and to examine its regulation by evaluating the expression of B-cell lymphoma leukemia-2 (Bcl- 2) and P53 proteins. We also sought to explore the relationships between cell apoptosis and GM-CSF, a cytokine able to increase eosinophil and macrophage survival. Methods: Apoptosis in eosinophils, macrophages, and T lymphocytes was evaluated in bronchial biopsy specimens obtained from 30 asthmatic subjects, 26 subjects with chronic bronchitis, and 15 control subjects by combining the terminal deoxynucleotidyl transferase-mediated dNTP nick end-labeling technique and immunohistochemistry. The expression of P53, Bcl-2, and GM-CSF was studied through immunohistochemistry by using specific mAbs. Results: The number of apoptotic eosinophils and macrophages was lower in subjects with asthma than in those with chronic bronchitis (P < .007 and P < .001, respectively) and inversely correlated with the clinical severity of asthma (P < .001 and P < .002, respectively). Few T lymphocytes were apoptotic in all groups studied. In asthma GM-CSF+ cells correlated with the number of nonapoptotic eosinophils and macrophages (P = .0001) and with the severity of the disease (P < .003). In asthma Bcl-2+ cells were higher than in control subjects and subjects with chronic bronchitis (P < .002 and P < .015, respectively), they outnumbered P53+ cells, and they correlated with the number of T lymphocytes (P < .001) and with the severity of the disease (P < .003). Conclusion: Airway inflammation in asthma is associated with an e nhanced survival of different cell types caused by reduced apoptosis.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
