Pulmonary alveolar macrophage function during acute inflammatory lung injury.
Pulmonary alveolar macrophage function during acute inflammatory lung injury.
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DOI：
10.1164/arrd.1987.135.6.1300
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发表时间：
2015-05
期刊：
影响因子：
--
通讯作者：
J. Brieland;R. Kunkel;J. Fantone
中科院分区：
文献类型：
--
作者：
J. Brieland;R. Kunkel;J. Fantone
肺泡巨噬细胞（PAM）在急性肺炎症中存在，但这些细胞在肺损伤的发生和消退中的功能作用尚不清楚。为了更好地了解PAM功能反应与急性可逆性肺损伤演变之间的关系，我们在无病原体的Sprague-Dawley大鼠中通过反向被动Arthus反应，在急性肺损伤开始后的特定时间点（0、6、12、24、48和72 h）检测了未刺激和刺激（PMA、zymosan） PAM分泌活性氧代谢产物（超氧阴离子O2-）和溶酶体酶（溶菌酶、n-乙酰- b - d -氨基葡萄糖酶）的能力。急性肺损伤后，与未损伤肺的PAM相比，受刺激的PAM产生更多的O2-。肺损伤后24 h， PAM产生最大的O2-，此时PMA和zymosan刺激PAM产生的O2-分别增加3.5倍和50%。在接下来的48小时内，这些细胞产生的O2-数量缓慢下降。受损肺部PAM产生O2-的增强不是由于产生O2的NADPH氧化酶的酶活性改变，也不是由于“活化”PAM中NADPH氧化酶的绝对增加。这些观察结果表明，损伤肺中PAM产生的O2增加是由于诱导氧化酶活性的机制增强。急性肺损伤后，PAM对溶菌酶和n -乙酰- b - d -氨基葡萄糖苷酶活性的积累和分泌存在差异。（摘要删节250字）
Pulmonary alveolar macrophages (PAM) are present during acute lung inflammation, yet the functional role of these cells in both the initiation and resolution of lung injury is not well defined. To better understand the relationship between PAM functional responses and the evolution of acute reversible lung injury, we examined the ability of both unstimulated and stimulated (PMA, zymosan) PAM to secrete reactive oxygen metabolites (superoxide anion O2-) and lysosomal enzymes (lysozyme, N-acetyl-B-D-glucosaminidase) at specific time points (0, 6, 12, 24, 48, and 72 h) after initiation of acute lung injury via reverse passive Arthus reaction in pathogen-free Sprague-Dawley rats. After acute lung injury, stimulated PAM produced increasing amounts of O2- compared with PAM from noninjured lungs. Maximal O2- production by PAM occurred at 24 h after lung injury, at which time a 3.5-fold and 50% increase in O2- production by PAM was observed when PAM were stimulated with PMA and zymosan, respectively. The amount of O2- generated by these cells slowly decreased during the next 48 h. Enhanced generation of O2- by PAM from injured lungs was not due to altered enzymatic activity of the O2--producing NADPH oxidase, nor was it due to an absolute increase in the NADPH oxidase in "activated" PAM. These observations suggest that increased O2- generation by PAM from injured lungs is due to enhancement of mechanisms responsible for induction of oxidase activity. In addition, a differential accumulation and secretion of lysozyme and N-acetyl-B-D-glucosaminidase activity by PAM was observed after acute lung injury.(ABSTRACT TRUNCATED AT 250 WORDS)