EARLY IDENTIFICATION OF INTERLEUKIN-16 (LYMPHOCYTE CHEMOATTRACTANT FACTOR) AND MACROPHAGE INFLAMMATORY PROTEIN 1-ALPHA (MIP1-ALPHA) IN BRONCHOALVEOLAR LAVAGE FLUID OF ANTIGEN-CHALLENGED ASTHMATICS

Accumulation of CD4(+) interleukin (IL)-2R(+) lymphocytes in the airwa ys of asthmatics is generally attributed to the presence of chemoattra ctant cytokines. The precise mechanism for the initiation of the earli est CD4(+) lymphocyte infiltration and activation is unknown. In this study, we describe for the first time the presence of lymphocyte chemo attractant activity in the bronchoalveolar lavage (BAL) fluid obtained from asthmatics 6 h after antigen challenge. The majority of the chem oattractant activity at this early time point is represented by IL-16 (lymphocyte chemoattractant factor), a CD4(+) cell-specific chemoattra ctant and growth factor. In addition to IL-16, macrophage inflammatory protein la (MIP1 alpha) chemotactic bioactivity was detected in signi ficant levels. While IL-16, MIP1 alpha, and IL-8 were all identified b y enzyme-linked immunosorbent assay, the great majority of the lymphoc yte chemoattractant activity in the BAL fluid after antigen challenge is attributable to IL-16 and MIP1 alpha. There were no detectable leve ls of IL-16 nor MIP1 alpha in BAL fluid of antigen-challenged normal s ubjects nor atopic nonasthmatics nor in saline-challenged lobes from t he asthmatics. The identification of multiple lymphocyte chemoattracta nts early after antigen challenge suggests a complex cellular, as well as chemoattractant cytokine, profile in initiating the CD4(+) T cell- mediated inflammatory process that is specific for the atopic asthmati c phenotype.