AIRWAY MACROPHAGES FROM PATIENTS WITH ASTHMA DO NOT PROLIFERATE

Background. Macrophages are involved in asthma, but their pulmonary tu rnover is unknown. We compared the ability of bronchoalveolar lavage ( BAL) and bronchial macrophages to proliferate in normal subjects and p atients with asthma. Methods: BAL cells from eight patients with asthm a and eight normal volunteers were separated with a discontinuous Perc oll gradient (Pharmacia Fine Chemicals, Uppsala, Sweden). In a first e xperiment, nuclei of each alveolar macrophage (AM) fraction, stained w ith propidium iodide, were analyzed for DNA content with a flow cytome ter, and the proportions of cells in the G0/G1, S, and G2 + M phases w ere determined. In a second experiment, expression of Ki-67-related an tigen was sought on AMs by immunocytochemistry. Macrophages from 10 pa tients with asthma and 10 normal volunteers were studied in biopsy spe cimens by means of immunohistochemistry with a panmacrophage monoclona l antibody (HAM-56) and a monoclonal antibody against proliferating ce ll nuclear antigen. Results: The proportions of BAL AMs in the differe nt phases of the cell cycle were similar in normal subjects and patien ts with asthma for all fractions, and the percentage of cells in S and G2 +/- M phases ranged from 7.3% to 11.3%. Under 1% of BAL AMs expres sed Ki-67-related antigen. None of the macrophages present in the biop sy specimens expressed proliferating cell nuclear antigen. Conclusions : This study does not indicate that an important source of airway macr ophages is local proliferation.