PT  - JOURNAL ARTICLE
AU  - C. Laflamme
AU  - E. Israël-Assayag
AU  - Y. Cormier
TI  - Apoptosis of bronchoalveolar lavage lymphocytes in hypersensitivity pneumonitis
AID  - 10.1183/09031936.03.00283903
DP  - 2003 Feb 01
TA  - European Respiratory Journal
PG  - 225--231
VI  - 21
IP  - 2
4099  - http://erj.ersjournals.com/content/21/2/225.short
4100  - http://erj.ersjournals.com/content/21/2/225.full
SO  - Eur Respir J2003 Feb 01; 21
AB  - The aim of this study was to look at the apoptosis of alveolar lymphocytes in hypersensitivity pneumonitis (HP). HP patients and normal unexposed controls were studied. The percentage of apoptotic lymphocytes was significantly lower in HP patients than in normal patients (37.4±3.4 versus 56.5±5.5% for Annexin V and propidium iodine detection methods and 0.4±0.1 versus 1.0±0.2% for dUTP nick end-labelling technique (TUNEL)). The proportion of bronchoalveolar lavage (BAL) lymphocytes positive for Fas antigen was significantly higher in HP patients than in normal subjects (71.7±5.4 versus 50.4±9.0%). However, no significant difference was found in the proportion of BAL lymphocytes positive for Fas ligand (FasL) between the two groups. Soluble Fas (sFas) levels in the BAL fluid of the patients and normals were 80.5±8.5 pg·mL−1 and 23.2±3.1 pg·mL−1, respectively. A positive correlation was found between the percentage of BAL lymphocytes and the levels of sFas for the total subjects but not within the separate study groups. The intracellular quantity of the inducible anti-apoptotic gene Bcl-xL product was significantly higher in the pulmonary lymphocytes of HP patients than in lymphocytes of the control, while no difference was found for constitutive anti-apoptotic protein (Bcl–2). In conclusion, the apoptosis of pulmonary lymphocytes is lower in hypersensitivity pneumonitis than in normal subjects. This could be explained, at least in part, by an increase of soluble Fas, the anti-apoptic gene, and Bcl-xL.