title: [Lymphocyte apoptosis in asthmatic patients and its molecular mechanism].
abstract: OBJECTIVE
  To assess the apoptosis rate of peripheral blood lymphocytes isolated from patients with asthma and explore its molecular mechanism.
  
  
  METHODS
  Lymphocytes were isolated with ficoll-hypaque gradient method and T lymphocytes were further isolated with nylon pili. T lymphocytes were stimulated by anti- CD3+ antibody for 0, 24, 48, 72 hours in vitro and the apoptosis rates were measured with in situ tailing technique. At the same time, Bcl-2 gene expression and Bax gene expression were observed with in situ hybridization.
  
  
  RESULTS
  The percentages of apoptosis cell in T lymphocytes from patients with asthma were significantly decreased and the timing delayed in comparison with those in normal controls (P < 0.01). The Bcl-2 mRNA expression in T lymphocytes was significantly increased in different time points than in normal controls (P < 0.01), but Bax mRNA expression in T lymphocytes was remarkably decreased (P < 0.01). The rates of Bcl-2/Bax mRNA could not reach the state of the controls until 72 hours from the begining of the stimulation with the anti-CD3+.
  
  
  CONCLUSIONS
  The inhibited apoptosis might be one of the reasons for the chronic persistent inflammation in the airways in asthmatic patients and the imbalance between Bcl-2 gene expression and Bax gene expression may be one of the molecular mechanisms for the inhibited apoptosis.
authors.affiliation: Department of Respiratory Disease, Tongji Hospital, Tongji Medical University, Wuhan 430030.
authors.forename: J
authors.initials: J
authors.lastname: Xue
authors.forename: Y
authors.initials: Y
authors.lastname: Xu
authors.forename: Z
authors.initials: Z
authors.lastname: Zhang
mesh_terms: D000328:Adult; D017209:Apoptosis; D001249:Asthma / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006801:Humans; D020287:In Situ Nick-End Labeling; D008297:Male; D008854:Microscopy, Electron; D013601:T-Lymphocytes / Q000473:pathology* / Q000648:ultrastructure