Blunt chest trauma induces delayed splenic immunosuppression
Blunt chest trauma induces delayed splenic immunosuppression
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DOI：
10.1097/01.shk.0000127684.64611.5c
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发表时间：
2004-07-01
期刊：
影响因子：
3.1
通讯作者：
Gebhard, F
中科院分区：
文献类型：
--
作者：
Knöferl, MW;Liener, UC;Gebhard, F
严重的钝性胸部创伤常伴有多器官功能衰竭和脓毒症。创伤后免疫抑制似乎在他们的发展中发挥了重要作用。然而，肺挫伤后的免疫学改变并不充分阐明。具体而言，尚不清楚远离撞击部位的免疫活性细胞是否受到影响。因此，我们的目的是表征肺挫伤对淋巴细胞和脾巨噬细胞的影响。将雄性C3 H/HeN小鼠（n = 8-10只/组）麻醉并进行创伤或假手术。钝性胸部创伤是由集中在胸部的冲击波引起的。2或24 h后，分离脾细胞和脾巨噬细胞并刺激48 h。通过ELISA定量从脾细胞以及从脾巨噬细胞（TNF-α、IL-10、IL-12、IL-18）释放的细胞因子（IFN-γ、IL-2、IL-3、IL-10、IL-12、IL-18）以及TNF-α和IL-6的血浆水平。结果表明，在钝性胸部创伤后2 h，血浆TNF-α和IL-6显著升高。同时，未检测到脾细胞细胞因子产生的差异。然而，在24小时，在创伤动物中观察到显著抑制的细胞因子释放。此外，脾巨噬细胞在创伤后24 h显示出TNF-α、IL-10和IL-12的产生显著减少，而IL-18的释放在创伤后2 h显著增加。这些结果表明，钝性胸部创伤导致严重的淋巴细胞和脾巨噬细胞的免疫功能障碍。因此，肺挫伤作为一种局部类型的创伤导致免疫活性细胞群的功能障碍，这些免疫活性细胞群位于远离损伤部位。
Severe blunt chest trauma is frequently associated with multiple organ failure and sepsis. Posttraumatic immunosuppression seems to play a major role in their development. However, the immunologic alterations following pulmonary contusion are insufficiently elucidated. Specifically, it remains unknown whether immunocompetent cells located distant from the site of the impact are affected. We therefore aimed to characterize the influence of pulmonary contusion on lymphocytes and splenic macrophages. Male C3H/HeN mice (n = 8-10/group) were anesthetized and subjected to trauma or sham procedure. Blunt chest trauma was induced by a blast wave focused on the thorax. Two or 24 h later, splenocytes and splenic macrophages were isolated and stimulated for 48 h. The cytokine release (IFN-gamma, IL-2, IL-3, IL-10, IL-12, IL-18) from splenocytes as well as from splenic macrophages (TNF-alpha, IL-10, IL-12, IL-18) and plasma levels of TNF-alpha and IL-6 were quantified by ELISA. The results indicate that at 2 h after blunt chest trauma, plasma TNF-alpha and IL-6 were markedly increased. At the same time, no differences in splenocyte cytokine production were detectable. However, at 24 h a significantly depressed cytokine release was observed in trauma animals. Furthermore, splenic macrophages showed a significantly decreased production of TNF-alpha, IL-10, and IL-12 at 24 h and markedly increased release of IL-18 at 2 h after trauma. These results indicate that blunt chest trauma causes severe immunodysfunction of lymphocytes and splenic macrophages. Thus, lung contusion as a localized type of trauma causes dysfunction of immunocompetent cell populations, which are located distant from the site of injury.