Beltrán-García Jesús, Osca-Verdegal Rebeca, Jávega Beatriz, Herrera Guadalupe, O'Connor José-Enrique, García-López Eva, Casabó-Vallés Germán, Rodriguez-Gimillo María, Ferreres José, Carbonell Nieves, Pallardó Federico V, García-Giménez José Luis
Center for Biomedical Research Network on Rare Diseases (CIBERER), Carlos III Health Institute, 46010 Valencia, Spain.
INCLIVA Biomedical Research Institute, 46010 Valencia, Spain.
Biomedicines. 2022 Feb 23;10(3):525. doi: 10.3390/biomedicines10030525.
(1) Background: Sepsis is a life-threatening condition caused by an abnormal host response to infection that produces altered physiological responses causing tissue damage and can result in organ dysfunction and, in some cases, death. Although sepsis is characterized by a malfunction of the immune system leading to an altered immune response and immunosuppression, the high complexity of the pathophysiology of sepsis requires further investigation to characterize the immune response in sepsis and septic shock. (2) Methods: This study analyzes the immune-related responses occurring during the early stages of sepsis by comparing the amounts of cytokines, immune modulators and other endothelial mediators of a control group and three types of severe patients: critically ill non-septic patients, septic and septic shock patients. (3) Results: We showed that in the early stages of sepsis the innate immune system attempts to counteract infection, probably via neutrophils. Conversely, the adaptive immune system is not yet fully activated, either in septic or in septic shock patients. In addition, immunosuppressive responses and pro-coagulation signals are active in patients with septic shock. (4) Conclusions: The highest levels of IL-6 and pyroptosis-related cytokines (IL-18 and IL-1α) were found in septic shock patients, which correlated with D-dimer. Moreover, endothelial function may be affected as shown by the overexpression of adhesion molecules such as s-ICAM1 and E-Selectin during septic shock.
(1) 背景:脓毒症是一种由宿主对感染的异常反应引起的危及生命的病症,会产生改变的生理反应,导致组织损伤,并可能导致器官功能障碍,在某些情况下还会导致死亡。尽管脓毒症的特征是免疫系统功能失调,导致免疫反应改变和免疫抑制,但脓毒症病理生理学的高度复杂性需要进一步研究,以明确脓毒症和脓毒性休克中的免疫反应特征。(2) 方法:本研究通过比较对照组以及三类重症患者(危重症非脓毒症患者、脓毒症患者和脓毒性休克患者)的细胞因子、免疫调节剂和其他内皮介质的量,分析脓毒症早期阶段发生的免疫相关反应。(3) 结果:我们发现,在脓毒症早期,先天性免疫系统可能通过中性粒细胞试图对抗感染。相反,在脓毒症患者和脓毒性休克患者中,适应性免疫系统尚未完全激活。此外,免疫抑制反应和促凝血信号在脓毒性休克患者中活跃。(4) 结论:在脓毒性休克患者中发现IL-6以及与细胞焦亡相关的细胞因子(IL-18和IL-1α)水平最高,这与D-二聚体相关。此外,脓毒性休克期间s-ICAM1和E-选择素等黏附分子的过表达表明内皮功能可能受到影响。