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Immunosuppressive Activity of Canine Pulmonary Surface Active Material¹

From the Respiratory Care Section, Department of Medicine, San Francisco Veterans Administration Hospital; and the Cardiovascular Research Institute, and the Departments of Medicine and Biochemistry, School of Medicine, University of California, San Francisco 94143

Abstract

The effects of canine surface active material (SAM), a lipoprotein unique to the lung, on the proliferative response of lymphocytes to immune stimulation were investigated. Peripheral blood lymphocytes were cultured in the presence of either endobronchial lavage fluid or purified SAM extracted from such lavage fluids. Cultures were stimulated with mitogens (Con-A, or PWM) or allogeneic cells (MLC), and the proliferative responses were measured by the uptake of tritiated thymidine.

Culture of lymphocytes in autologous endobronchial lavage fluid resulted in a suppressed response to all three stimuli: MLC (33% control response), PWM (54% control), Con-A (75% control). Culture of lymphocytes with purified SAM produced a dose-dependent inhibition of the responses to these stimuli (MLC > PWM > Con-A). Fifty percent inhibition of lymphocyte responses to MLC, PWM, or Con-A was produced by 4.2, 7.5, or 12.5 µg protein/ml of purified SAM, respectively. Supraoptimal doses of mitogens failed to alter the observed inhibitory activities. SAM was not cytotoxic for lymphocytes in these experiments. SAM was most inhibitory when added to lymphocytes at the time of mitogen stimulation; progressively less inhibition was produced by SAM added at increasing intervals of time after stimulation. Lymphocytes preincubated with SAM for 24 or 48 hr, washed, and then cultured in fresh medium displayed persistently suppressed responses.

These results demonstrate that canine SAM is a potent suppressor of lymphocyte proliferation in vitro. In vivo, SAM is found only in the lung and, during fetal development, is secreted by the lung into amniotic fluid. The presence of SAM in these locations may have important implications for our understanding of pulmonary and maternal-fetal immunology.

Footnotes

¹ This work was supported by research funds from the Veterans Administration and by National Institutes of Health Grant AI-12296, NHLBI Program Project Grant HL-06285, and Pulmonary SCOR Grant HL-19185 from the United States Public Health Service.

² Requests for reprints should be addressed to Dr. Michael Ansfield, Respiratory Care Section (111D), San Francisco Veterans Administration Hospital, 4150 Clement Street, San Francisco, California 94121.

³ Postdoctoral Research Trainee supported by National Institutes of Health Graduate Training Grant HL-07185.

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