1
15] we propose a model in which SP-A regulates host defense function by both indirect and direct mechanisms. The indirect effects, as documented in this study, comprise a broad-based regulation of levels of expression of a number of BAL proteins important for innate immunity and host defense function. In the K. pneumoniae model employed here these deficits were rapidly reversed by the infectious c
1
15] we propose a model in which SP-A regulates host defense function by both indirect and direct mechanisms. The indirect effects, as documented in this study, comprise a broad-based regulation of levels of expression of a number of BAL proteins important for innate immunity and host defense function. In the K. pneumoniae model employed here these deficits were rapidly reversed by the infectious c