Effects of surfactant protein A and surfactant lipids on lymphocyte proliferation in vitro

Abstract

We studied the effects of dipalmitoyl L-alpha-phosphatidylcholine (DPPC), Survanta, surfactant protein A (SP-A), and mixtures of these substances on mitogen-induced lymphocyte proliferation using concanavalin A as a mitogen. A concentration-dependent suppression of proliferation was observed with 50-250 micrograms/ml of DPPC or Survanta. However, when SP-A was added to cultures, proliferation was stimulated. The inhibitory effects of DPPC and Survanta were altered in mixtures that contained SP-A. When added to 50 micrograms/ml of Survanta, SP-A reversed the inhibitory influence of Survanta and caused increased proliferation. These findings suggest that surfactant phospholipids cause a suppression of mitogen-induced lymphocyte proliferation, which is reversed somewhat by addition of SP-A. We hypothesize that immune cell function in the lung varies with changes in the relative amounts of surfactant components. Changes in surfactant composition may occur during pulmonary inflammation or infection or with surfactant replacement therapy and may influence immune and inflammatory processes in the lung.

Effects of Surfactant Lipids and Surfactant Protein A on Host Defense Functions of Rat Alveolar Macrophages

“…have shown that immune cell functions can be modulated by a balance between SP-A and surfactant lipids. They demonstrated that SP-A increases cell surface marker expression in a monocytic cell line (37), augments TNF-␣ secretion by splenocytes (38), and stimulates mitogen-induced lymphocyte proliferation (39). SP-A-induced increases were inhibited by surfactant lipids, yet maintained under certain conditions by modifying the SP-A:lipid ratio.…”

Surfactant protein-A levels increase during Pneumocystis carinii pneumonia in the rat

“…A number of recent in vitro studies have suggested that SP-A might be involved in pulmonary host-defence, and in phagocytosis in particular [11][12][13][14][15][16][17][18], and an interaction between SP-A and P. carinii has been demonstrated [20]. Preliminary studies suggest that although SP-A may stimulate the in vitro phagocytosis of some organisms [10,11,15], such as Candida albicans, Staphylococcus aureus and Herpes simplex, it may interfere with the phagocytosis of P. carinii by alveolar macrophages [10].…”

“…The possibility that SP-A might modulate phagocyte function has been supported by recent in vitro experiments [10][11][12][13][14][15][16], although little is known about its role in vivo. In addition, recent studies from our laboratory have demonstrated that SP-A can also influence immune cell function by stimulating mitogen-induced proliferation and cytokine production [17,18].…”

The Pulmonary Surfactant System: Biochemical and Clinical Aspects

“…The presence of SP-A potentiates the antibacterial functions of alveolar macrophages [177] by modulating the immune cell function in the lung by regulating the cytokine production and immunoglobulin secretion [176].…”