Bidani A, Wang C Z, Heming T A
Department of Internal Medicine, University of Texas Medical Branch, Galveston, USA.
Burns. 1996 Mar;22(2):101-6. doi: 10.1016/0305-4179(95)00096-8.
Alveolar macrophage (AM) dysfunctions have been implicated in the pathogenesis of smoke inhalation lung injury. We investigated the early (within 70 min) effects of smoke inhalation on AM. The cells were recovered by bronchoalveolar lavage from rabbits ventilated with cotton smoke for 5 min followed by O2/room air for 60 min (smoke-exposed) or with room air in place of smoke (control). Smoke injury caused arterial blood carboxyhaemoglobin levels to increase 11-fold and reduced arterial blood PO2 (measured approximately 1 h postinjury) by 25 per cent. Scanning electron micrographs revealed denudation of plasmalemmal pseudopods in smoke-exposed AM. Smoke exposure suppressed both AM adherence to plastic and phagocytosis of opsonized bacteria. Basal superoxide (O2-) production was elevated in smoke-exposed AM, compared with controls, whereas PMA-stimulated O2- production was unaffected. Smoke-exposed AM had reduced basal secretion of tumour necrosis factor-alpha (TNF-alpha), but displayed a greater TNF response to stimulation with LPS than did control cells. LPS-stimulated TNF-alpha releases from control and smoke-exposed AM were suppressed by phosphodiesterase inhibitors pentoxifylline and theophylline, and were enhanced by the lipoxygenase inhibitor, MK886. The early responses of AM to smoke inhalation lung injury are consistent with activation of O2- production and priming of TNF-alpha release, concurrent with a functional down regulation of phagocytosis.
肺泡巨噬细胞（AM）功能障碍与烟雾吸入性肺损伤的发病机制有关。我们研究了烟雾吸入对AM的早期（70分钟内）影响。通过支气管肺泡灌洗从兔子中回收细胞，这些兔子用棉烟通气5分钟，然后用氧气/室内空气通气60分钟（烟雾暴露组）或用室内空气代替烟雾（对照组）。烟雾损伤导致动脉血中碳氧血红蛋白水平增加11倍，并使动脉血氧分压（在损伤后约1小时测量）降低25%。扫描电子显微镜照片显示，烟雾暴露的AM中质膜伪足剥脱。烟雾暴露抑制了AM对塑料的黏附以及对调理素化细菌的吞噬作用。与对照组相比，烟雾暴露的AM中基础超氧化物（O2-）生成增加，而佛波酯刺激的O2-生成不受影响。烟雾暴露的AM中肿瘤坏死因子-α（TNF-α）的基础分泌减少，但与对照细胞相比，对脂多糖刺激的TNF反应更大。磷酸二酯酶抑制剂己酮可可碱和茶碱抑制了对照组和烟雾暴露组AM中脂多糖刺激的TNF-α释放，而脂氧合酶抑制剂MK886增强了这种释放。AM对烟雾吸入性肺损伤的早期反应与O2-生成的激活、TNF-α释放的启动一致，同时伴有吞噬功能的下调。
