Nonalcoholic fatty liver disease aggravates acute pancreatitis through bacterial translocation and cholesterol metabolic dysregulation in the liver and pancreas in mice

Background:Nonalcoholic fatty liver disease(NAFLD)is an independent risk factor for severe acute pancreatitis(AP).The underlying mechanism remains unclear.We sought to determine how bacterial translocation and cholesterol metabolism in the liver and pancreas affect the severity of AP in NAFLD mice.Methods:C57BL/6N mice were fed on a high-fat diet(HFD)to generate the NAFLD model,and mice in the control group were provided with a normal diet(ND).After being anesthetized with ketamine/xylazine,mice got a retrograde infusion of taurocholic acid sodium into the pancreatic duct to induce AP,and sham operation(SO)was used as control.Serum amylase and Schmidt’s pathological score system were used to evaluate AP severity.Bacterial loads,total cholesterol level,and cholesterol metabolic-associated molecules[low-density lipoprotein receptor(LDLR)and ATP-binding cassette transporter A1(ABCA1)]were analyzed in the liver and pancreas.Results:Compared with the ND-AP group,mice in the HFD-AP group had severer pancreatitis,manifested with higher serum amylase levels and higher AP pathologic scores,especially the inflammation and hemorrhage scores.Compared with the HFD-SO group and ND-AP group,bacterial loads in the liver and pancreas were significantly higher in the HFD-AP group.Mice in the HFD-AP group showed a decreased LDLR expression and an increased ABCA1 expression in the pancreas,although there was no significant difference in pancreas total cholesterol between the HFD-AP group and the ND-AP group.Conclusions:NAFLD aggravates AP via increasing bacterial translocation in the liver and pancreas and affecting pancreas cholesterol metabolism in mice.

Over-starvation aggravates intestinal injury and promotes bacterial and endotoxin translocation under high-altitude hypoxic environment

AIM:To study whether over-starvation aggravates intestinal mucosal injury and promotes bacterial and endotoxin translocation in a high-altitude hypoxic environment.METHODS:Sprague-Dawley rats were exposed to hy-pobaric hypoxia at a simulated altitude of 7000 m for 72 h.Lanthanum nitrate was used as a tracer to detect intestinal injury.Epithelial apoptosis was observed with terminal deoxynucleotidyl transferase dUTP nick end labeling staining.Serum levels of diamino oxidase(DAO),malondialdehyde(MDA),glutamine(Gln),superoxide dismutase(SOD) and endotoxin were measured in intestinal mucosa.Bacterial translocation was detected in blood culture and intestinal homogenates.In addition,rats were given Gln intragastrically to observe its protective effect on intestinal injury.RESULTS:Apoptotic epithelial cells,exfoliated villi and inflammatory cells in intestine were increased with edema in the lamina propria accompanying effusion of red blood cells.Lanthanum particles were found in the intercellular space and intracellular compartment.Bacterial translocation to mesenteric lymph nodes(MLN) and spleen was evident.The serum endotoxin,DAO and MDA levels were significantly higher while the serum SOD,DAO and Gln levels were lower in intestine(P< 0.05).The bacterial translocation number was lower in the high altitude hypoxic group than in the high altitude starvation group(0.47±0.83 vs 2.38±1.45,P<0.05).The bacterial translocation was found in each organ,especially in MLN and spleen but not in peripheral blood.The bacterial and endotoxin translocations were both markedly improved in rats after treatment with Gln.CONCLUSION:High-altitude hypoxia and starvation cause severe intestinal mucosal injury and increase bacterial and endotoxin translocation,which can be treated with Gln.

Inhibitory effects of high-dose methylprednisolone on bacterial translocation from gut and endotoxin release following acute spinal cord injury-induced paraplegia in rats

BACKGROUND： Previous studies have shown that autonomic dysfunction results in gastrointestinal motility disorders and ultimately results in bacterial translocation following acute spinal cord injury （SCI）. Intensive methylprednisolone dosing improves neurological recovery in SCI patients. However, it remains uncertain whether high-dose methylprednisolone inhibits bacterial translocation and endotoxin release following acute SCI. OBJECTIVE： To investigate the inhibitory effect of methylprednisolone on bacterial translocation and endotoxin release from the gut in paraplegic rats. DESIGN, TIME AND SETTING： The randomized, controlled study was performed at the Orthopedic Lab, First Affiliated Hospital, Nanchang University, China, from April to December 2008. MATERIALS： Methylprednisolone （Pfizer, USA）, automatic microbial identification instrument ATB Expression and reagent ID 32 system （BioMerieux, France）, Limulus test kit （ACC, USA）, and optical microscope （Olympus, Japan） were used in this study. METHODS： A paraplegia model was established following SCI in 48 Wistar rats, aged 7 weeks. The rats were equally and randomly assigned to saline and methylprednisolone groups. Immediately post-injury, the methylprednisolone group was administered 30 mg/kg methylprednisolone via caudal intravenous infusion, followed by a 23-hour infusion of 5.4 mg/kg per hour. The saline group received an equal volume of saline as placebo. MAIN OUTCOME MEASURES： At 24 hours, 72 hours, and 1 week after SCI, blood samples were collected for bacterial cultures, and bacteria and endotoxin were identified using ATB Expression and Limulus test kits. In addition, mesenteric lymph node, spleen, and liver samples were collected for bacterial cultures. Histological examinations of mesenteric lymph node, spleen, liver, jejunum, and ileum were performed 1 week post-injury. Locomotor function in the hind limb was evaluated using the Basso, Beattie, and Bresnahan score at pre-injury time point, as well as 24 hours, 72 hours, and 1 week post-injury. RESULTS： Endotoxemia and bacterial growth were identified at 24 hours post-injury in both groups. However, plasma endotoxin levels were significantly decreased in the methylprednisolone group compared with the saline group at 72 hours and 1 week post-injury （P 〈 0.05）. Translocated bacteria mainly comprised Bacillus coli, Enterobacter cloacae, Escherichia coli, Proteus vulgaris, and Enterococcus faecalis following SCI combined with paraplegia. Histological changes were not as severe in the methylprednisolone group compared with the saline group 1 week after injury. Basso, Beattie, and Bresnahan scores were significantly better in the methylprednisolone group compared with the saline group 1 week after injury （P 〈 0.05）. CONCLUSION： High-dose methylprednisolone inhibited bacterial translocation from the gut and endotoxin release in rats with SCI.

Role of intestinal bifidobacteria in the pathogenesis of gut-derived bacteria/endotoxin translocation and the effect of bifidobacterial supplement on gut barrier function following burns

Objective:Early multiple organ dysfunction syndrome appears to be facilitated with bacterial transloca-tion in severely burn injury,yet the mechanisms of bacterial translocation remains in dispute.The aim of this studywas to investigate the potential role of intestinal bifidobacteria in the pathogenesis of gut-derived bacteria/endotoxintranslocation following burns and the effects of bifidohacterial supplement on gut barrier.Methods:Wistar rats wererandomly divided into burn group(Burn,n=60),sham burn g...

Influence of splanchnic vascular infusion on the content of endotoxins in plasma and the translocation of intestinal bacteria in rats with acute hemorrhage necrosis pancreatitis

INTRODUCTIONThe main reason for the death of the patient with acutehemorrhage necrosis pancreatitis(AHNP)is pancreaticinfection and multi-organ failure caused by endotoxemiaand intestinal bacterial translocation.However,thepathogenesis of endotoxemia and intestinal

Microbiota and the gut-liver axis:Bacterial translocation,inflammation and infection in cirrhosis

Liver disease is associated with qualitative and quantitative changes in the intestinal microbiota.In cirrhotic patients the alteration in gut microbiota is characterized by an overgrowth of potentially pathogenic bacteria(i.e.,gram negative species)and a decrease in autochthonous familiae.Here we summarize the available literature on the risk of gut dysbiosis in liver cirrhosis and its clinical consequences.We therefore described the features of the complex interaction between gut microbiota and cirrhotic host,the so called"gut-liver axis",with a particular attention to the acquired risk of bacterial translocation,systemic inflammation and the relationship with systemic infections in the cirrhotic patient.Such knowledge might help to develop novel and innovative strategies for the prevention and therapy of gut dysbiosis and its complication in liver cirrhosis.

Relationship between enteric microecologic dysbiosis and bacterial translocation in acute necrotizing pancreatitis

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Effect of artesunate supplementation on bacterial translocation and dysbiosis of gut microbiota in rats with liver cirrhosis

AIM: To evaluate the effect of artesunate(AS) supplementation on bacterial translocation(BT) and gut microbiota in a rat model of liver cirrhosis. METHODS: Fifty-four male Sprague-Dawley rats were randomly divided into a normal control group(N), a liver cirrhosis group(M) and a liver cirrhosis group intervened with AS(MA). Each group was sampled at 4, 6 and 8 wk. Liver cirrhosis was induced by injection of carbon tetrachloride(CCl4), intragastric administration of 10% ethanol, and feeding a high fat diet. Rats in the MA group were intragastrically administered with AS(25 mg/kg body weight, once daily). Injuries of the liver and intestinal mucosa were assessed by hematoxylineosin or Masson's trichrome staining. Liver index was calculated as a ratio of the organ weight(g) to body weight(g). The gut microbiota was examined by automated ribosomal intergenic-spacer analysis of fecal DNA. BT was assessed by standard microbiological techniques in the blood, mesenteric lymph nodes(MLNs), liver, spleen, and kidney. RESULTS: Compared to group N, the body weight was reduced significantly in groups M and MA due to the development of liver cirrhosis over the period of 8 wk. The body weight was higher in group MA than in group M. The liver indices were significantly elevated at 4, 6 and 8 wk in groups M and MA compared to group N. AS supplementation partially decreased the liver indices in group MA. Marked histopathologic changes in the liver and small intestinal mucosa in group M were observed, which were alleviated in group MA. Levels of pro-inflammatory interleukin-6 and tumor necrosis factor-α were significantly elevated at 8 wk in ileal homogenates in group M compared to group N, which were decreased after AS supplementation in group MA. The dysbiosis of gut microbiota indicated by the mean diversity(Shannon index) and mean similarity(Sorenson index) was severe as the liver cirrhosis developed, and AS supplementation had an apparent intervention effect on the dysbiosis of gut microbiota at 4 wk. The occurrence of BT was increased in the liver of group M compared to that of group N. AS supplementation reduced BT in group MA at 8 wk. BT also occurred in the MLNs, spleen, and kidney, which was reduced by AS supplementation. BT was not detected in the blood in any group.CONCLUSION: Dysbiosis of gut microbiota, injury of intestinal mucosal barrier and BT occurred as liver cirrhosis progressed, which might enhance inflammation and aggravate liver injury. AS may have other nonantimalarial effects that modulate gut microbiota,inhibit BT and alleviate inflammation, resulting in a reduction in CCl4, alcohol and high fat-caused damages to the liver and intestine.

Early intrajejunal nutrition: bacterial translocation and gut barrier function of severe acute pancreatitis in dogs

Objective: To evaluate the effect of early intrajejunalnutrition in attenuating bacterial and/or endotoxintranslocation and improving gut barrier function ofsevere acute pancreatitis (SAP) in dogs.Methods: 15 dogs were divided into parenteral nutrition(PN) group(7 dogs)and early intrajejunal nutrition(EIN) group(8). EIN was delivered nutrients via a nee-dle jejunostomy catheter feeding at 48h after operation.SAP model was induced by injecting 1 ml/kg of com-bined solution of 5% sodium taurocholate and 8000-10000 BAEE units trypsin/ml into the pancreas via thepancreatic duct. Systemic blood samples were ob-tained before and 1, 3, 5, 7 d following SAP, and culturedby aerobic as well as anaerobic bacterial growth. Systemicplasma and portal vein endotoxin levels were quantifiedby the chromogenic limulus amebocyte lysate (LAL)technique. Portal vein blood and specimens of tissuefrom the mesenteriolum and mesocolon lymph nodes,lung, pulmonary portal lymph nodes, pancreatitis tissueand periopancreas tissue were adopted before the experi-ment was finished. Aliquots of the homogenata were cul-tured as blood mentioned above to determine the magnitudeof the bacteria DNA, protein and the villi, the thickness ofmucosa, and the whole bowel wall of the ileum and trans-verse colon were measured.Results: The study showed that the levels of systemicplasma endotoxin and the magnitude of bacterialtranslocation to the portal and systemic blood and dis-tant organ were reduced significantly in the EINgroup as compared with the TPN group. The contentsof protein and DNA, the height of villi, the thicknessof mucosa and whole bowel wall of the ileum andtransverse colon in the EIN group were higher thanthose in the PN group.Conclusion: Our results suggested that EIN is safe andeffective to be adopted by intrajejunal delivery of nu-trients in SAP, decreases the occurrence of gut bacterialtranslocation, and improves the gut barrier function.

Tracing method study of bacterial translocation in vivo

INTRODUCTIONEndogenesis infection plays an important role innosocomial infection.By studying progress ofbacteria translocation from intestinal tract,theconcept of gut-origin infection has been acceptedgradually.Because of no ideal tracing method,there were some controversies.In order to solve theproblem,the PUC19 plasmid vector tracing

Effects of glutamine and curcumin on bacterial translocation in jaundiced rats

AIM: To investigate the effect of curcumin on bacterial translocation and oxidative damage in an obstructive jaundice model and compare the results to glutamine, an agent known to be effective and clinically used. METHODS: Twenty-four female Wistar-Albino rats, weighing 200-250 g, were randomly divided into three groups (8 in each group). After ligation of the common bile duct in all animals, GroupⅠ received oral normal saline, Group Ⅱ received oral glutamine and Group Ⅲ received oral curcumin for seven days. Blood samples via cardiac puncture, tissue samples (terminal ileum, liver and mesenteric lymph node) and peritoneal fluid were obtained from the animals at the time of death to investigate bacterial translocation and oxidative damage. RESULTS: We observed that both glutamine and curcumin reduced bacterial translocation in blood, hepatocellular damage, plasma cytokine levels, oxidative tissue damage and apoptosis significantly compared to the control group. Additionally, glutamine showed protective effects on ileal epithelium and reduced villus atrophy. CONCLUSION: On the basis of these findings, both curcumin and glutamine are thought to be effective in preventing or reducing bacterial translocation and oxidative damage in obstructive jaundice.

Effects of recombinant human growth hormone on intestinal translocation of bacteria and endotoxin in rats with obstructive jaundice

Extrahepatic biliary obstruction promotes intestinal translocation of bacteria and endotoxin and this process is an important cause of morbidity and mortality in patients with jaundice. This study was undertaken to investigate the effect and mechanism of recombinant human growth hormone (rhGH) and to alleviate intestinal translocation of bacteria and endotoxin in murine obstructive jaundice. METHODS:A group of 42 Wistar rats were divided into 3 groups:sham operation (SO), bile duct ligation (BDL), and BDL and rhGH treatment (rhGH). By the end of the experiment,on day 7, the animals were killed, and their liver function and serum endotoxin were measured, bacterial cultures of the liver, kidney and mesenchymal lymph were made. Terminal ileum mucosa was observed under an electron microscope. RESULTS:Liver function was improved more significantly in the rhGH group than in the BDL group. The value of endotoxin in the rhGH group was 0.38±0.03 EU/ml, significantly lower than that in the BDL group (0.65±0.04 EU/ml, P【0.01), and similar to that in the SO group (0.30±0.02 EU/ml, P】0.05). The rate of bacteria translocation in the liver, kidney and mesenteric lymph was much higher in the BDL group than in other two groups. The rate of bacteria translocation in mesenteric lymph was 64.29%,significantly higher than that in the SO group and the rhGH group (P【0.05). There was no significant difference in bacteria translocation rate between the SO group and the rhGH group (P】0.05). Under an electron microscope , ileum mucosa epithelial cells in the BDL group were necrotic, and organelle were markedly metamorphic. In the rhGH group, ultrastructural changes were less evident or similar to those in the SO group. CONCLUSION:rhGH has significant protective effects on intestinal mucosa barrier in obstructive jaundice, and reduces intestinal translocation of bacteria and endotoxin.

Gut flora and bacterial translocation in chronic liver disease

增加的证据建议内脏植物群的精神错乱具有到有肝硬化的病人的实质的临床的关联。特别地，肠的细菌的增生和从肠的腔的内脏植物群的增加的细菌的易位在这个组为细菌的感染预先安排到一个增加的潜力。最近的研究建议除了他们在公开易传染的事件的致病和败血的临床的后果的角色，内脏植物群甚至当公开感染不在时贡献肝硬化的支持 inflammatory 状态。而且，内脏植物群的操作可以有利在肝脏硬化症的病人影响肝功能与更病原的潜力在损坏另外的内脏植物群种类的情况下扩充乳的酸类型的细菌的肠的内容。这里，我们在这个组考察在内脏植物群，细菌的易位，细菌的感染，支持 inflammatory cytokine 生产和肝功能之间的各种各样的相互关系的当前的概念。

Protective effects of terminal ileostomy against bacterial translocation in a rat model of intestinal ischemia/reperfusion injury

AIM:To investigate the effects of terminal ileostomy on bacterial translocation(BT)and systemic inflammation after intestinal ischemia/reperfusion(I/R)injury in rats.METHODS:Thirty-two rats were assigned to either the sham-operated group,I/R group,I/R+resection and anastomosis group,or the I/R+ileostomy group.The superior mesenteric artery was occluded for 60 min.After 4 h,tissue samples were collected for analysis.BT was assessed by bacteriologic cultures,intestinal permeability and serum levels of endotoxin;systemic inflammation was assessed by serum levels of tumornecrosis factor(TNF)-α,interleukin(IL)-6 and IL-10,as well as by the activity of myeloperoxidase(MPO)and by intestinal histopathology.RESULTS:Intestinal I/R injury not only caused morphologic damage to ileal mucosa,but also induced BT,increased MPO activity and promoted the release of TNF-α,IL-6,and IL-10 in serum.BT and ileal mucosa injuries were significantly improved and levels of TNF-αand IL-6 in serum were decreased in the I/R+ileostomy group compared with the I/R+resection and anastomosis group.CONCLUSION:Terminal ileostomy can prevent the detrimental effects of intestinal I/R injury on BT,intestinal tissue,and inflammation.

Using the polymerase chain reaction coupled with denaturing gradient gel electrophoresis to investigate the association between bacterial translocation and systemic inflammatory response syndrome in predicted acute severe pancreatitis

AIM: To investigate the use of PCR and DGGE to investigate the association between bacterial translocation and systemic inflammatory response syndrome in predicted severe AP.METHODS: Patients with biochemical and clinical evidence of acute pancreatitis and an APACHE Ⅱ score ≥8 were enrolled. PCR and DGGE were employed to detect bacterial translocation in blood samples collected on d1,3, and 8 after the admission. Standard microbial blood cultures were taken when there was clinical evidence of sepsis or when felt to be clinically indicated by the supervising team.RESULTS: Six patients were included. Of all the patients investigated, only one developed septic complications;the others had uneventful illness. Bacteria were detected using PCR in 4 of the 17 collected blood samples. The patient with sepsis was PCR-positive in two samples (taken on d 1 and 3), despite three negative blood cultures. Using DGGE and specific primers, the bacteria in all blood specimens which tested positive for the presence of bacterial DNA were identified as E coli.CONCLUSION: Our study confirmed thatunlike traditional microbiological techniques, PCR can detect the presence of bacteria in the blood of patients with severe AP. Therefore, this latter method in conjunction with DGGE is potentially an extremely useful tool in predicting septic morbidity and evaluating patients with the disease. Further research using increased numbers of patients, in particular those patients with necrosis and sepsis, is required to assess the reliability of PCR and DGGE in the rapid diagnosis of infection in AP.

Leaky gut and the liver: A role for bacterial translocation in nonalcoholic steatohepatitis

Gut flora and bacterial translocation (BT) play important roles in the pathogenesis of chronic liver disease, including cirrhosis and its complications. Intestinal bacterial overgrowth and increased bacterial translocation of gut flora from the intestinal lumen predispose patients to bacterial infections, major complications and also play a role in the pathogenesis of chronic liver disorders. Levels of bacterial lipopolysaccharide, a component of gram-negative bacteria, are increased in the portal and/or systemic circulation in several types of chronic liver disease. Impaired gut epithelial integrity due to alterations in tight junction proteins may be the pathological mechanism underlying bacterial translocation. Preclinical and clinical studies over the last decade have suggested a role for BT in the pathogenesis of nonalcoholic steatohepatitis (NASH). Bacterial overgrowth, immune dysfunction, alteration of the luminal factors, and altered intestinal permeability are all involved in the pathogenesis of NASH and its complications. A better understanding of the cell-specific recognition and intracellular signaling events involved in sensing gut-derived microbes will help in the development of means to achieve an optimal balance in the gut-liver axis and ameliorate liver diseases. These may suggest new targets for potential therapeutic interventions for the treatment of NASH. Here, we review some of the mechanisms connecting BT and NASH and potential therapeutic developments.

Effect of honey on bacterial translocation and intestinal morphology in obstructive jaundice

AIM:To evaluate the effects of honey on bacterial translocation and intestinal villus histopathology in experimental obstructive jaundice.METHODS:Thirty Wistar-Albino rats were randomly divided into three groups each including 10 animals:group Ⅰ,sham-operated;group Ⅱ,ligation and section of the common bile duct(BDL);group Ⅲ,bile duct ligation followed by oral supplementation of honey(BDL+honey) 10 g/kg per day.Liver,blood,spleen,mesenteric lymph nodes,and ileal samples were taken for microbiological,light and transmission electrone microscopic examination.RESULTS:Although the number of villi per centimeter and the height of the mucosa were higher in sham group,there was no statistically significant difference between sham and BDL + honey groups(P>0.05).On the other hand,there was a statistically significant difference between BDL group and other groups(P<0.05).The electron microscopic changes werealso different between these groups.Sham and honey groups had similar incidence of bacterial translocation(P>0.05).BDL group had significantly higher rates of bacterial translocation as compared with sham and honey groups.Bacterial translocation was predominantly detected in mesenteric lymph nodes.CONCLUSION:Supplementation of honey in presence of obstructive jaundice ameliorates bacterial translocation and improves ileal morphology.

Melatonin reduces bacterial translocation and apoptosis in trinitrobenzene sulphonic acid-induced colitis of rats

AIM: To investigate the effects of exogenous melatonin on bacterial translocation and apoptosis in a rat ulcerati-ve colitis model. METHODS: Rats were randomly assigned to three groups: groupⅠ: control, group Ⅱ: experimental colitis, group Ⅲ: colitis plus melatonin treatment. On d 11 after colitis, plasma tumor necrosis factor-α, portal blood endotoxin levels, colon tissue myeloperoxidase and caspase-3 activity were measured. Bacterial translocation was quantified by blood, lymph node, liver and spleen culture. RESULTS: We observed a significantly reduced inciden-ce of bacterial translocation to the liver, spleen, mesen-teric lymph nodes, portal and systemic blood in animals treated with melatonin. Treatment with melatonin signifi-cantly decreased the caspase-3 activity in colonic tissues compared to that in trinitrobenzene sulphonic acid-trea-ted rats (16.11 ± 2.46 vs 32.97 ± 3.91, P < 0.01). CONCLUSION: Melatonin has a protective effect on ba-cterial translocation and apoptosis.

Bacterial Translocation and Change in Intestinal Permeability in Patients after Abdominal Surgery

The purpose of this study was to investigate bacterial translocation and change in intestinal permeability in patients after abdominal surgery. Sixty-three patients undergoing elective abdominal surgery were enrolled in the study. Blood samples were collected prior to operation and 2, 24, 48 h after surgery for bacterial culture, microbial DNA extraction, plasma D-lactate and endotoxin measurement. PCR analysis was performed after DNA extraction, with β-lactosidase gene of E. coli and 16S rRNA gene as target genes. All patients were observed for a period of 30 days for infectious complications. Our results showed that no bacterial DNA was detected before surgery, but after operation it was found in 12 patients （19.0%）. Bacterial DNA was detected in 41.7% （10/24） of SIRS patients and 5.1% （2/39） of non-SIRS patients （P〈0.01）. About 83.3% of PCR-positive patients developed systemic inflammatory response syndrome （SIRS）, but only 27.5% of PCR-negative patients did so （P〈0.01）. Two thirds of PCR-positive patients developed infectious complications, while none of PCR-negative patients did （P〈0.01）. The blood culture was positive only in 3 patients （4.8%）, who were all PCR-positive. E. coli DNA was found in 66.7% of the PCR-positive patients. The plasma levels of D-lactate and endotoxin were elevated significantly 2, 24 and 48 h after operation in PCR-positive patients, with a significant positive correlation found between them （r=0.91, P〈0.01）. It is concluded that increased intestinal permeability was closely related with bacterial translocation. Intestinal bacterial translocation （most commonly E. coli） might occur at early stage （2 h） after abdominal surgery. Postoperative SIRS and infection might bear a close relationship with bacterial translocation.

Liver Cirrhosis and Intestinal Bacterial Translocation

Intestinal barrier dysfunction, facilitating translocation of bacteria and bacterial products, plays an important role in the pathophysiology of liver cirrhosis and its complications. Intestinal defense system including microbial barrier, immunologic barrier, mechanical barrier, chemical barrier, plays an important role in the maintenance of intestinal function. Under normal circumstances, the intestinal barrier can prevent intestinal bacteria through the intestinal wall from spreading to the body. Severe infection, trauma, shock, cirrhosis, malnutrition, immune suppression conditions, intestinal bacteria and endotoxin translocation, can lead to multiple organ dysfunction. The intestinal microflora is not only involved in the digestion of nutrients, but also in local immunity, forming a barrier against pathogenic microorganisms. The derangement of the gut microflora may lead to microbial translocation, defined as the passage of viable microorganisms or bacterial products from the intestinal lumen to the mesenteric lymph nodes and other extraintestinal sites. In patients with cirrhosis, primary and intestinal flora imbalance, intestinal bacterial overgrowth, intestinal mucosal barrier dysfunction, endotoxemia is associated with weakened immunity.