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AJP - Lung Cellular and Molecular Physiology, Vol 273, Issue 4 831-L839, Copyright © 1997 by American Physiological Society
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S. R. Bates, J. Xu, C. Dodia and A. B. Fisher
Institute for Environmental Medicine, School of Medicine, University of Pennsylvania, Philadelphia 19104-6068, USA.
The current study examined whether long-term culture of macrophages affects their metabolism of surfactant components. Compared with freshly isolated resting macrophages in culture for 1 h, macrophages attached to plastic dishes for 24 h showed evidence of conversion to a "primed" state with 1) an altered morphology characterized by a larger size, ruffled membranes, lamellipodia, and a "foamy" appearance after attachment to glass and 2) a fivefold greater respiratory burst in response to phorbol 12-myristate 13-acetate stimulation. On incubation with iodinated surfactant protein A (SP-A), the 24-h alveolar or tissue macrophages showed a 5- or a 23-fold greater increase in SP-A degradation, respectively, than macrophages cultured for 1 h. Conditioned media experiments demonstrated that the elevated rate of SP-A degradation after prolonged culture was not a result of proteases secreted by the macrophages. Incubation of cells with NH4Cl reduced the degradation of SP-A to a similar extent (to 33% of control values) in resting and primed tissue macrophages. On the other hand, length of time of cell culture did not affect macrophage uptake and degradation of [3H]dipalmitoylphosphatidylcholine in mixed unilamellar liposomes. Thus freshly isolated resting tissue and alveolar macrophages can be primed to specifically increase their rate of SP-A degradation. Activation of macrophages associated with lung disease may be important for SP-A metabolism and surfactant function.
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