Yun Zhang1, Jian Zhang1, Tao Xu1, Wei Wu2, Fang-Fang Huang3, Wen-Qiao Yu1, Shao-Yang Zhang1, Ting-Bo Liang4. 1. Department of Hepatobiliary and Pancreatic Surgery, the Second Affiliated Hospital, College of Medicine Zhejiang University, Hangzhou, Zhejiang, China. 2. 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. 3. Department of Surgical Intensive Care Unit, the First Affiliated Hospital, College of Medicine Zhejiang University, Hangzhou, Zhejiang, China. 4. Department of Hepatobiliary and Pancreatic Surgery, the Second Affiliated Hospital, College of Medicine Zhejiang University, Hangzhou, Zhejiang, China. Electronic address: liangtingbo2005@gmail.com.
Abstract
BACKGROUND: 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. METHODS: 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. RESULT: 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). CONCLUSION: 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.
BACKGROUND: 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. METHODS: 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. RESULT: 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). CONCLUSION: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.