ROLE OF SURFACTANT PROTEIN-A IN THE PATHOGENESIS OF TUBERCULOSIS IN SUBJECTS WITH HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION

Human immunodeficiency virus (HIV)-infected subjects are at increased risk for tuberculosis even before there is a significant loss of CD4 l ymphocytes. A factor was found to be present in the bronchoalveolar la vage (BAL) of HIV-infected subjects that promoted the attachment of M. tuberculosis (MTB) organisms to alveolar macrophages (AMs). Using Cr- 51-labeled MTB organisms, BAL from control subjects resulted in MTB at tachment to AMs at 11.6% +/- 1.0%; in contrast, BAL from HIV-infected subjects increased attachment to 33.1% +/- 3.8% (P < 0.001). Surfactan t protein A (SP-A) levels in BAL of normal controls was 1.9 +/- 0.3 mu g/ml and was 5.5 +/- 0.4 mu g/ml in the BAL of HIV-infected subjects (P < 0.01). When SP-A was removed by immunoprecipitation from the BAL of HIV-infected subjects, MTB attachment decreased from 33.1% +/- 3.8% to 11.3% +/- 0.4% (P < 0.001), a value identical to control levels. E xogenous human SP-A (5 mu g/ml) was added back to the immunoprecipitat ed BAL and the enhanced attachment of MTB was restored. These data sug gest that BAL from HIV-infected subjects contain a factor that facilit ates MTB attachment to AMs, the first critical step in the establishme nt of infection. This factor appears to be SP-A.