Bankey P E, Williams J G, Guice K S, Taylor S N
University of Texas Southwestern Medical Center, Dallas, USA.
Surgery. 1995 Aug;118(2):431-8; discussion 438-9. doi: 10.1016/s0039-6060(05)80355-1.
Thermal injury induces circulating levels of interleukin-6 (IL-6). The liver and lung have been proposed as major sources of IL-6 after injury; however, multiple cell types within these organs are capable of IL-6 production. In these experiments we further characterize cellular sources of IL-6 after thermal injury by examining tissue macrophage response in the liver and lung and IL-6 production of cultured pulmonary microvascular endothelial cells (PMECs).
Serum, liver and lung tissue, and tissue macrophage IL-6 response was determined in Wistar rats subjected to a 35 to 40% total body surface area scald injury. Cultured PMEC IL-6 production was determined after treatment with serum from the burned animals. IL-6 bioactivity was assayed by 7TD1 proliferation, and IL-6 messenger RNA levels were determined by reverse transcriptase-polymerase chain reaction. Alveolar macrophages were obtained by bronchoalveolar lavage. Kupffer cells and PMECs were obtained by enzyme digestion of liver and lungs.
Burn increases circulating IL-6 activity through postburn day 3 (388 +/- 50 units/0.1 ml versus 80 +/- 12 units/0.1 ml in controls). Burn increases lung and liver IL-6 messenger RNA without concurrent increase in the alveolar macrophages or Kupffer cells and persists in the lung after bronchoalveolar lavage. PMECs cultured in the presence of postburn day 3 serum (10% vol) release more IL-6 activity (1118 +/- 333 units/culture versus sham rat serum with 288 +/- 146 units/culture) than control cultures and have more readily detectable levels of IL-6 messenger RNA.
Non-tissue macrophage sources including microvascular endothelium may be a contributing source of IL-6 in the lung after thermal injury.
热损伤可诱导循环中的白细胞介素-6（IL-6）水平升高。肝脏和肺被认为是损伤后IL-6的主要来源；然而，这些器官内的多种细胞类型都能够产生IL-6。在这些实验中，我们通过检测肝脏和肺中的组织巨噬细胞反应以及培养的肺微血管内皮细胞（PMECs）的IL-6产生情况，进一步明确热损伤后IL-6的细胞来源。
对全身表面积35%至40%烫伤的Wistar大鼠测定血清、肝脏和肺组织以及组织巨噬细胞的IL-6反应。用烧伤动物的血清处理后，测定培养的PMECs的IL-6产生情况。通过7TD1增殖测定IL-6生物活性，通过逆转录聚合酶链反应测定IL-6信使核糖核酸水平。通过支气管肺泡灌洗获得肺泡巨噬细胞。通过肝脏和肺的酶消化获得库普弗细胞和PMECs。
烧伤后3天内循环中的IL-6活性增加（388±50单位/0.1毫升，而对照组为80±12单位/0.1毫升）。烧伤增加了肺和肝脏的IL-6信使核糖核酸水平，而肺泡巨噬细胞或库普弗细胞没有同时增加，并且在支气管肺泡灌洗后肺中仍持续存在。在烧伤后第3天的血清（10%体积）存在下培养的PMECs释放的IL-6活性（1118±333单位/培养物，而假手术大鼠血清为288±146单位/培养物）比对照培养物更多，并且IL-6信使核糖核酸水平更容易检测到。
包括微血管内皮细胞在内的非组织巨噬细胞来源可能是热损伤后肺中IL-6的一个促成来源。
