Zhang Yun, Zhang Jian, Xu Tao, Wu Wei, Huang Fang-Fang, Yu Wen-Qiao, Zhang Shao-Yang, Liang Ting-Bo
Department of Hepatobiliary and Pancreatic Surgery, the Second Affiliated Hospital, College of Medicine Zhejiang University, Hangzhou, Zhejiang, China.
State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Institute of Infectious Diseases, the First Affiliated Hospital, College of Medicine Zhejiang University, Hangzhou, Zhejiang, China.
Surgery. 2017 Feb;161(2):546-555. doi: 10.1016/j.surg.2016.08.029. Epub 2016 Oct 4.
Intestinal dendritic cells play important roles in regulating the function of the intestinal immune barrier and the intestinal bacterial translocation. In this study, we aim to investigate the effects of allicin on the function of mesenteric lymph node-dendritic cells after trauma/hemorrhagic shock.
One hundred and eight-four Sprague-Dawley rats were randomly assigned into a sham group (n = 46), sham + allicin group (n = 46), trauma/hemorrhagic shock group (n = 46), and trauma/hemorrhagic shock + allicin group (n = 46). Studies were performed on an in vivo model of spontaneously breathing rats with induced trauma/hemorrhagic shock. Allicin was diluted in resuscitation fluid and was administered through the right jugular vein. Flow cytometry was used to determine the expression of CD80, CD86, and major histocompatibility complex II (MHC II) on the surface of mesenteric lymph node-dendritic cells, as well as apoptosis. Intraintestinal bacterial translocation was monitored by using bioluminescent citrobacter. Intestinal permeability tests were conducted by using both FITC-Dextran and Ussing-Chember assay.
CD80 and MHC-II expression levels were downregulated in the trauma/hemorrhagic shock group compared with the sham and sham + allicin groups; however, the expression was upregulated after allicin treatment. Also, allicin could ameliorate the trauma/hemorrhagic shock-induced increase in early apoptosis of mesenteric lymph node-dendritic cells. A significant increase was observed in the permeability of the intestinal barrier after severe traumatic shock, along with an obvious intraintestinal bacterial translocation to mesenteric lymph node. No difference was noticed in the bacterial translocation in mesenteric lymph node in the trauma/hemorrhagic shock group compared with trauma/hemorrhagic shock + allicin group (P = .589), which indicated allicin could not block bacterial translocation into mesenteric lymph node after trauma/hemorrhagic shock. However, it may increase the capacity of mesenteric lymph node to block intraintestinal bacterial translocation to extraintestinal organs as a statistical difference was noticed in the bacterial translocation in liver, blood, and spleen between trauma/hemorrhagic shock and trauma/hemorrhagic shock + allicin groups (P < .05).
Trauma/hemorrhagic shock resulted in a decrease of mature mesenteric lymph node-dendritic cells. Allicin treatment could block intraintestinal bacterial translocation through increasing the immunologic barrier function of mesenteric lymph node by modulating dendritic cells maturation.
肠道树突状细胞在调节肠道免疫屏障功能和肠道细菌移位中发挥重要作用。在本研究中，我们旨在探讨大蒜素对创伤/失血性休克后肠系膜淋巴结树突状细胞功能的影响。
184只Sprague-Dawley大鼠随机分为假手术组（n = 46）、假手术+大蒜素组（n = 46）、创伤/失血性休克组（n = 46）和创伤/失血性休克+大蒜素组（n = 46）。在诱导创伤/失血性休克的自主呼吸大鼠体内模型上进行研究。大蒜素用复苏液稀释后经右颈静脉给药。采用流式细胞术检测肠系膜淋巴结树突状细胞表面CD80、CD86和主要组织相容性复合体II（MHC II）的表达以及细胞凋亡情况。使用生物发光柠檬酸杆菌监测肠道细菌移位。采用异硫氰酸荧光素-葡聚糖（FITC-Dextran）和尤斯灌流小室法进行肠道通透性检测。
与假手术组和假手术+大蒜素组相比，创伤/失血性休克组CD80和MHC-II表达水平下调；然而，大蒜素治疗后表达上调。此外，大蒜素可改善创伤/失血性休克诱导的肠系膜淋巴结树突状细胞早期凋亡增加。严重创伤性休克后肠道屏障通透性显著增加，同时肠道细菌明显移位至肠系膜淋巴结。创伤/失血性休克组与创伤/失血性休克+大蒜素组肠系膜淋巴结细菌移位无差异（P = 0.589），这表明大蒜素不能阻止创伤/失血性休克后细菌移位至肠系膜淋巴结。然而，它可能增加肠系膜淋巴结阻止肠道细菌移位至肠外器官的能力，因为创伤/失血性休克组与创伤/失血性休克+大蒜素组肝脏、血液和脾脏细菌移位存在统计学差异（P < 0.05）。
创伤/失血性休克导致成熟的肠系膜淋巴结树突状细胞减少。大蒜素治疗可通过调节树突状细胞成熟增加肠系膜淋巴结的免疫屏障功能，从而阻止肠道细菌移位。
