Evaluation of apoptosis of eosinophils, macrophages, and T lymphocytes in mucosal biopsy specimens of patients with asthma and chronic bronchitis

J Allergy Clin Immunol. 1999 Apr;103(4):563-73. doi: 10.1016/s0091-6749(99)70225-3.


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 enhanced survival of different cell types caused by reduced apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Apoptosis*
  • Asthma / pathology
  • Asthma / physiopathology*
  • Biopsy
  • Bronchi / pathology*
  • Bronchitis / pathology
  • Bronchitis / physiopathology*
  • CD36 Antigens / biosynthesis
  • Chronic Disease
  • Eosinophils / physiology*
  • Gene Expression Regulation
  • Granulocyte-Macrophage Colony-Stimulating Factor / biosynthesis
  • Humans
  • Immunohistochemistry
  • In Situ Nick-End Labeling
  • Macrophages / physiology*
  • Middle Aged
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • T-Lymphocytes / physiology*
  • Tumor Suppressor Protein p53 / biosynthesis
  • Tumor Suppressor Protein p53 / genetics


  • CD36 Antigens
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53
  • Granulocyte-Macrophage Colony-Stimulating Factor