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 lymphocytes. A factor was found to be present in the bronchoalveolar lavage (BAL) of HIV-infected subjects that promoted the attachment of M. tuberculosis ( MTB) organisms to alveolar macrophages (AMs). Using 51Cr-labeled MTB organisms, BAL from control subjects resulted in MTB attachment to AMs at 11.6% +/- 1.0%; in contrast, BAL from HIV-infected subjects increased attachment to 33.1% +/- 3.8% (P < 0.001). Surfactant protein A ( SP-A) levels in BAL of normal controls was 1.9 +/- 0.3 micrograms/ml and was 5.5 +/- 0.4 micrograms/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. Exogenous human SP-A (5 micrograms/ml) was added back to the immunoprecipitated BAL and the enhanced attachment of MTB was restored. These data suggest that BAL from HIV-infected subjects contain a factor that facilitates MTB attachment to AMs, the first critical step in the establishment of infection. This factor appears to be SP-A.[1]References
- Role of surfactant protein A in the pathogenesis of tuberculosis in subjects with human immunodeficiency virus infection. Martin, W.J., Downing, J.F., Williams, M.D., Pasula, R., Twigg, H.L., Wright, J.R. Proc. Assoc. Am. Physicians (1995) [Pubmed]
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