Pulmonary surfactant modulation of host-defense function

In the lung, there are mechanisms for host-defense similar to those that are operational elsewhere in the body, but there are also mechanisms that are unique to the lung. Some of these additional mechanisms involve pulmonary surfactant. There is mounting evidence that the surfactant proteins, SP-A and SP-D, both of which are collagenous C-type lectins or collectins, are involved in the recognition of some microorganisms. In some cases these proteins function as opsonins and stimulate chemotaxis and phagocytosis. However, there is considerable selectivity in this process. The effects of these proteins vary depending on the type of microorganism, the specific strain involved, the growth phase of the pathogen, and the phagocytic cell type tested. Several other aspects of immune cell function have also been investigated in this regard. These include proliferative activity in response to a variety of stimuli, the production of cytokines, and the secretion of immunoglobulin. In all cases the predominant surfactant lipids had inhibitory or anti-inflammatory effects. Recently these observations have been extended to include some of the commonly used surfactant replacement preparations. SP-A stimulates some of the same processes that are inhibited by the surfactant lipids. Some of the minor lipid components of surfactant can also have stimulatory activity. These opposite effects on immune cell function by different surfactant components suggest that the relative abundance of various surfactant components in the alveolar lining material determines the functional status of immune cells in the lung. These studies also raise the possibility that alterations in surfactant could play a role in the pathogenesis of some lung diseases involving immune cells.