Surfactant protein A stimulation of inflammatory cytokine and immunoglobulin production

Pulmonary surfactant plays a variety of roles related to the regulation of immune function in the lung. Of particular interest in this regard is surfactant protein A (SP-A), a calcium-dependent lectin. We have reported previously that SP-A enhances concanavalin A-induced proliferation, and in this study we examined the secretion of tumor necrosis factor-α (TNF-α), interleukins 1α, 1β, and 6, and interferon-γ by human peripheral blood mononuclear cells. Levels of all of the cytokines except interferon-γ were increased by SP-A. In rat peripheral blood cells, splenocytes, and alveolar macrophages we found a similar enhancement of TNF-α release by SP-A. In combinations of SP-A and surfactant lipids, the increased levels of TNF-α resulting from SP-A treatment decreased as the lipids increased. At higher relative concentrations of SP-A, the lipids had little or no effect. SP-A also enhanced the production of immunoglobulins A, G, and M by rat splenocytes. Levels of each isotype were increased severalfold over control levels. These data demonstrate that SP-A is capable of modulating immune cell function in the lung by regulating cytokine production and immunoglobulin secretion.