Division of Critical Care Medicine, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Division of Pathology and Laboratory Medicine, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio.
Shock. 2018 Nov;50(5):557-564. doi: 10.1097/SHK.0000000000001076.
Severe sepsis and septic shock are the biggest cause of mortality in critically ill patients. Obesity today is one of the world's greatest health challenges. Little is known about the extent of involvement of the white adipose tissue (WAT) in sepsis and how it is being modified by obesity. We sought to explore the involvement of the WAT in sepsis. We hypothesize that sepsis induces browning of the WAT and that obesity alters the response of WAT to sepsis. Six-week-old C57BL/6 mice were randomized to a high-fat diet to induce obesity (obese group) or control diet (nonobese group). After 6 to 11 weeks of feeding, polymicrobial sepsis was induced by cecal ligation and puncture (CLP). Mice were sacrificed at 0, 18, and 72 h after CLP and epididymal WAT (eWAT), inguinal WAT, and brown adipose tissue (BAT) harvested. Both types of WAT were processed for light microscopy and transmission electron microscopy to assess for morphological changes in both obese and nonobese mice. Tissues were processed for immunohistochemistry, image analyses, and molecular analyses. BATs were used as a positive control. Nonobese mice have an extensive breakdown of the unilocular lipid droplet and smaller adipocytes in WAT compared with obese mice after sepsis. Neutrophil infiltration increases in eWAT in nonobese mice after sepsis but not in obese mice. Nonobese septic mice have an increase in mitochondrial density compared with obese septic mice. Furthermore, nonobese septic mice have an increase in uncoupling protein-1 expression. Although the WAT of nonobese mice have multiple changes characteristic of browning during sepsis, these changes are markedly blunted in obesity.
严重脓毒症和感染性休克是危重病患者死亡的最大原因。肥胖是当今世界面临的最大健康挑战之一。人们对白色脂肪组织(WAT)在脓毒症中的参与程度以及肥胖如何改变其对脓毒症的反应知之甚少。我们试图探讨 WAT 在脓毒症中的作用。我们假设脓毒症会诱导 WAT 的棕色化,而肥胖会改变 WAT 对脓毒症的反应。将 6 周龄的 C57BL/6 小鼠随机分为高脂肪饮食诱导肥胖组(肥胖组)或对照饮食组(非肥胖组)。喂养 6 至 11 周后,通过盲肠结扎和穿刺(CLP)诱导多微生物脓毒症。CLP 后 0、18 和 72 小时处死小鼠,采集附睾 WAT(eWAT)、腹股沟 WAT 和棕色脂肪组织(BAT)。对两种类型的 WAT 进行光镜和透射电镜检查,以评估肥胖和非肥胖小鼠的形态学变化。对组织进行免疫组织化学、图像分析和分子分析。BAT 用作阳性对照。与肥胖小鼠相比,非肥胖小鼠在脓毒症后 WAT 中可见大量的单室脂质滴破裂和较小的脂肪细胞。中性粒细胞浸润在非肥胖脓毒症小鼠的 eWAT 中增加,但在肥胖脓毒症小鼠中没有增加。非肥胖脓毒症小鼠的线粒体密度增加,而肥胖脓毒症小鼠的线粒体密度则减少。此外,非肥胖脓毒症小鼠的解偶联蛋白-1 表达增加。尽管非肥胖脓毒症小鼠的 WAT 发生了多种与棕色化相关的变化,但这些变化在肥胖小鼠中明显减弱。