title: Evaluation of apoptosis of eosinophils, macrophages, and T lymphocytes in mucosal biopsy specimens of patients with asthma and chronic bronchitis.
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).
  
  
  CONCLUSIONS
  Airway inflammation in asthma is associated with an enhanced survival of different cell types caused by reduced apoptosis.
authors: Istituto di Fisiopatologia Respiratoria, C.N.R., Via Trabucco, Palermo, Italy.
authors: A M
authors: AM
authors: Vignola
authors: P
authors: P
authors: Chanez
authors: G
authors: G
authors: Chiappara
authors: L
authors: L
authors: Siena
authors: A
authors: A
authors: Merendino
authors: C
authors: C
authors: Reina
authors: R
authors: R
authors: Gagliardo
authors: M
authors: M
authors: Profita
authors: J
authors: J
authors: Bousquet
authors: G
authors: G
authors: Bonsignore
mesh_terms: D000328:Adult; D017209:Apoptosis; D001249:Asthma / Q000473:pathology / Q000503:physiopathology*; D001706:Biopsy; D001980:Bronchi / Q000473:pathology*; D001991:Bronchitis / Q000473:pathology / Q000503:physiopathology*; D018955:CD36 Antigens / Q000096:biosynthesis; D002908:Chronic Disease; D004804:Eosinophils / Q000502:physiology*; D005786:Gene Expression Regulation; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000096:biosynthesis; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008264:Macrophages / Q000502:physiology*; D008875:Middle Aged; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D013601:T-Lymphocytes / Q000502:physiology*; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis / Q000235:genetics
chemical_list: D018955:CD36 Antigens; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D016178:Granulocyte-Macrophage Colony-Stimulating Factor