Macrophage and type II cell catabolism of SP-A and saturated phosphatidylcholine in mouse lungs
Macrophage and type II cell catabolism of SP-A and saturated phosphatidylcholine in mouse lungs
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DOI：
10.1152/ajplung.2001.280.6.l1266
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发表时间：
2001-06-01
影响因子：
4.9
通讯作者：
Jobe, AH
中科院分区：
文献类型：
--
作者：
Gurel, O;Ikegami, M;Jobe, AH
肺泡型细胞和巨噬细胞是参与肺表面活性物质肺泡清除和分解代谢的主要细胞。我们测定了小鼠体内II型细胞和巨噬细胞对饱和磷脂酰胆碱和表面活性蛋白A(SP-A)分解代谢的贡献。我们使用了气管内给药的SP-A，放射性标记的二棕榈酰磷脂酰胆碱([H-3]DPPC)，以及抗降解的类似物[C-14]DPPC-乙醚。分别于气管内注射后15min、7h、19h、29h、48h处死小鼠，进行肺泡灌洗，回收巨噬细胞和表面活性物质。未经灌洗恢复的II型细胞和巨噬细胞随后通过酶消化法分离肺组织。测定全肺、灌洗液巨噬细胞、肺泡灌洗液、肺泡液、肺泡灌洗液、肺泡灌洗液在根据II型细胞分离效率进行校正后，与巨噬细胞(灌洗液加肺消化液)和II型细胞相关联的I-125-扩乳醇-酪胺-SP-A和[C-14]DPPC-乙醚的数量大致相同。80%的巨噬细胞相关放射性标记是从肺消化的巨噬细胞中回收的。我们得出结论，巨噬细胞和II型细胞对小鼠饱和磷脂酰胆碱和SP-A的分解代谢具有同等的贡献。
Type II cells and macrophages are the major cells involved in the alveolar clearance and catabolism of surfactant. We measured type II cell and macrophage contributions to the catabolism of saturated phosphatidylcholine and surfactant protein A (SP-A) in mice. We used intratracheally administered SP-A labeled with residualizing I-125-dilactitol-tyramine, radiolabeled dipalmitoylphosphatidylcholine ([H-3] DPPC), and its degradation-resistant analog [C-14] DPPC-ether. At 15 min and 7, 19, 29, and 48 h after intratracheal injection, the mice were killed; alveolar lavage was then performed to recover macrophages and surfactant. Type II cells and macrophages not recovered by the lavage were subsequently isolated by enzymatic digestion of the lung. Radioactivity was measured in total lung, lavage fluid macrophages, alveolar washes, type II cells, and lung digest macrophages. Approximately equal amounts of I-125-dilactitol-tyramine-SP-A and [C-14] DPPC-ether associated with the macrophages (lavage fluid plus lung digest) and type II cells when corrected for the efficiency of type II cell isolation. Eighty percent of the macrophage-associated radiolabel was recovered from lung digest macrophages. We conclude that macrophages and type II cells contribute equally to saturated phosphatidylcholine and SP-A catabolism in mice.