Wu Huang-Pin, Shih Chi-Chung, Chu Chien-Ming, Huang Chih-Yu, Hua Chung-Ching, Liu Yu-Chih, Chuang Duen-Yau
Division of Pulmonary, Critical Care and Sleep Medicine, Chang Gung Memorial Hospital, Keelung, Taiwan; College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Department of Emergence, Chang Gung Memorial Hospital, Keelung, Taiwan.
J Formos Med Assoc. 2015 Dec;114(12):1250-7. doi: 10.1016/j.jfma.2014.09.009. Epub 2015 Jan 28.
BACKGROUND/PURPOSE: Interleukin (IL)-17 family members (IL-17A to IL-17F) are appearing to play key roles in host defense and inflammatory disease. Recently, several cytokines, such as IL-6, IL-10, IL-12, and transforming growth factor (TGF)-β1, were shown to have vital roles in severe sepsis. However, the influence of IL-17 on these cytokine responses from peripheral blood mononuclear cells (PBMCs) is unclear.
Fifty-two patients who were admitted to our intensive care unit (ICU) because of severe sepsis were enrolled into this study. To validate experimental findings, 25 healthy controls were enrolled. Lipopolysaccharide-stimulated PBMCs with IL-17 or anti-IL-17 treatments were cultured for 24 hours. IL-6, IL-10, IL-12, and TGF-β1 levels in supernatants were measured.
The IL-12 production from stimulated PBMCs was increased after IL-17 treatment in both control and patient groups. Additional treatment of anti-IL-17 enhanced IL-10 production but decreased IL-12 production from stimulated PBMCs of healthy controls and patients with severe sepsis.
IL-17 was helpful for inflammation in severe sepsis. Lack of IL-17 decreased IL-12 and enhanced IL-10 production from PBMCs, which resulted in immune imbalance.
背景/目的：白细胞介素（IL）-17家族成员（IL-17A至IL-17F）似乎在宿主防御和炎症性疾病中发挥关键作用。最近，几种细胞因子，如IL-6、IL-10、IL-12和转化生长因子（TGF）-β1，被证明在严重脓毒症中起重要作用。然而，IL-17对外周血单个核细胞（PBMCs）这些细胞因子反应的影响尚不清楚。
52例因严重脓毒症入住我们重症监护病房（ICU）的患者被纳入本研究。为了验证实验结果，纳入了25名健康对照者。用IL-17或抗IL-17处理脂多糖刺激的PBMCs并培养24小时。测量上清液中IL-6、IL-10、IL-12和TGF-β1的水平。
在对照组和患者组中，IL-17处理后刺激的PBMCs产生的IL-12增加。抗IL-17的额外处理增强了健康对照者和严重脓毒症患者刺激的PBMCs产生的IL-10，但降低了IL-12的产生。
IL-17有助于严重脓毒症中的炎症反应。缺乏IL-17会降低PBMCs产生的IL-12并增强IL-10的产生，从而导致免疫失衡。
