ALVEOLAR MACROPHAGE PHAGOCYTOSIS IS ENHANCED AFTER BLUNT CHEST TRAUMA AND ALTERS THE POSTTRAUMATIC MEDIATOR RELEASE
ALVEOLAR MACROPHAGE PHAGOCYTOSIS IS ENHANCED AFTER BLUNT CHEST TRAUMA AND ALTERS THE POSTTRAUMATIC MEDIATOR RELEASE
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DOI：
10.1097/shk.0b013e318234f8a0
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发表时间：
2011-12-01
期刊：
影响因子：
3.1
通讯作者：
Knoeferl, Markus W.
中科院分区：
文献类型：
--
作者：
Seitz, Daniel H.;Palmer, Annette;Knoeferl, Markus W.
钝性胸部创伤可引起短暂的中性粒细胞的肺部侵袭和肺泡上皮2型(AT2)细胞的凋亡。肺泡巨噬细胞(AM-Phi)可清除凋亡细胞。我们假设胸部创伤改变了AM Phi的吞噬反应以及吞噬过程中AM Phi的介质释放。为了研究这一点，雄性Spraogue-Dawley大鼠受到钝性胸部创伤。创伤后2小时或24小时分离的AM Phi用凋亡细胞或调理小球进行吞噬实验。创伤后2 h，未经刺激的AM phi对凋亡的AT2细胞的吞噬作用明显增强。伤后24小时，创伤动物AM Phi经佛波醇-12-肉豆蔻酸盐-13-乙酸酯刺激后，吞噬的中性粒细胞明显多于假手术动物。创伤后的肺泡巨噬细胞在加入乳胶珠后，其释放的肿瘤坏死因子α、巨噬细胞炎性蛋白1α和细胞因子诱导的中性粒细胞趋化因子1水平显著升高，而当它们摄取凋亡细胞时，其IL 1β和巨噬细胞炎性蛋白1α的水平显著降低。在体内，创伤大鼠气管内滴注乳胶珠的吞噬功能减少。闭合性胸部创伤后肺泡灌洗液中吞噬支持表面活性蛋白A和D的浓度略有下降，而AT2细胞表面活性蛋白DmRNA的表达在伤后2 h显著增加，提示胸部创伤后肺泡灌洗液中巨噬细胞吞噬功能明显增强。调理珠的吞噬作用增强了肺挫伤后的免疫反应，而对凋亡细胞的吞噬作用则下调了免疫反应。我们的数据强调了吞噬作用在肺挫伤后创伤后炎症中的重要作用。
Blunt chest trauma is known to induce a pulmonary invasion of short-lived polymorphonuclear neutrophils and apoptosis of alveolar epithelial type 2 (AT2) cells. Apoptotic cells are removed by alveolar macrophages (AM Phi). We hypothesized that chest trauma alters the phagocytic response of AM Phi as well as the mediator release of AM Phi during phagocytosis. To study this, male Sprague-Dawley rats were subjected to blunt chest trauma. Phagocytosis assays were performed in AM Phi isolated 2 or 24 h after trauma with apoptotic cells or opsonized beads. Phagocytosis of apoptotic AT2 cells by unstimulated AM Phi was significantly increased 2 h after trauma. At 24 h, AM Phi from traumatized animals, stimulated with phorbol-12-myristate-13-acetate, ingested significantly more apoptotic polymorphonuclear neutrophils than AM Phi from sham animals. Alveolar macrophages after trauma released significantly higher levels of tumor necrosis factor alpha, macrophage inflammatory protein 1 alpha, and cytokine-induced neutrophil chemoattractant 1 when they incorporated latex beads, but significantly lower levels of interleukin 1 beta and macrophage inflammatory protein 1 alpha when they ingested apoptotic cells. In vivo, phagocytosis of intratracheally instilled latex beads was decreased in traumatized rats. The bronchoalveolar lavage concentrations of the phagocytosis-supporting surfactant proteins A and D after blunt chest trauma were slightly decreased, whereas surfactant protein D mRNA expression in AT2 cells was significantly increased after 2 h. These findings indicate that chest trauma augments the phagocytosis of apoptotic cells by AM Phi. Phagocytosis of opsonized beads enhances and ingestion of apoptotic cells downregulates the immunologic response following lung contusion. Our data emphasize the important role of phagocytosis during posttraumatic inflammation after lung contusion.