Allicin ameliorates intraintestinal bacterial translocation after trauma/hemorrhagic shock in rats: The role of mesenteric lymph node dendritic cell
Allicin ameliorates intraintestinal bacterial translocation after trauma/hemorrhagic shock in rats: The role of mesenteric lymph node dendritic cell
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大蒜素改善大鼠创伤/失血性休克后肠内细菌移位：肠系膜淋巴结树突状细胞的作用
DOI：
10.1016/j.surg.2016.08.029
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发表时间：
2017-02
期刊：
影响因子：
3.8
通讯作者：
Liang Tingbo
中科院分区：
文献类型：
--
作者：
Huang Fangfang;Yu Wenqiao;Zhang Shaoyang;Liang Tingbo
背景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起重要作用。方法将184只SD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）。在具有诱导创伤/失血性休克的自主呼吸大鼠的体内模型上进行研究。将大蒜素稀释在复苏液中，并通过右颈静脉给药。流式细胞仪检测肠系膜淋巴结树突状细胞表面CD 80、CD 86和主要组织相容性复合物II（MHC II）的表达及细胞凋亡。用生物发光柠檬酸杆菌监测肠道细菌移位。结果创伤/失血性休克组CD 80和MHC-II表达水平较假手术组和假手术+大蒜素组明显下调，而大蒜素治疗后CD 80和MHC-II表达水平明显上调。大蒜素还可改善创伤/失血性休克诱导的肠系膜淋巴结树突状细胞早期凋亡的增加。严重创伤性休克后肠屏障通透性明显增加，肠内细菌沿着移位至肠系膜淋巴结。创伤/失血性休克组肠系膜淋巴结细菌移位与创伤/失血性休克+大蒜素组相比无显著性差异（P= 0.589），提示大蒜素不能阻断创伤/失血性休克后肠系膜淋巴结细菌移位。然而，大蒜素可增强肠系膜淋巴结阻断肠内细菌向肠外器官移位的能力，创伤/失血性休克组和创伤/失血性休克+大蒜素组肝、血、脾细菌移位率差异有统计学意义（P<0.05）。大蒜素通过调节树突状细胞的成熟，增强肠系膜淋巴结的免疫屏障功能，阻断肠道细菌移位。
BackgroundIntestinal 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.MethodsOne 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.ResultCD80 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).ConclusionTrauma/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.
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影响因子：
3
作者：
Feng Y;Zhu X;Wang Q;Jiang Y;Shang H;Cui L;Cao Y
通讯作者：
Cao Y
影响因子：
3.3
作者：
Fink, Mitchell P
通讯作者：
Fink, Mitchell P
影响因子：
4.2
作者：
Kyo, E;Uda, N;Itakura, Y
通讯作者：
Itakura, Y
影响因子：
4.4
作者：
Tinsley, KW;Grayson, MH;Hotchkiss, RS
通讯作者：
Hotchkiss, RS
DOI：
10.1097/ta.0b013e3181a8b286
发表时间：
2010-03
期刊：
The Journal of trauma
影响因子：
--
作者：
L. Liang;Guo-dong Xu;Yun Zhang;Wei Chen;Junjian Li;T. Liang
通讯作者：
L. Liang;Guo-dong Xu;Yun Zhang;Wei Chen;Junjian Li;T. Liang