Alcoholic liver disease is a leading cause of morbidity and liver-related death worldwide. Intestinal bacterial overgrowth and dysbiosis induced by ethanol ingestion play an important role in the pathogenesis of alcoholic liver disease. After exposure to alcohol in the lumen, enteric bacteria alter their metabolism and thereby disturb intestinal homeostasis. Disruption of the mucosal barrier results in the translocation of microbial products that contribute to liver disease by inducing hepatic inflammation. In this review, we will discuss the effects of alcohol on the intestinal microbiome, and in particular, its effects on bacterial metabolism, bacterial translocation and ecological balance. A better understanding of the interactions among alcohol, the host and the microbiome will reveal new targets for therapy and lead to new treatments.
Bacterial Translocation/physiology ; Central Nervous System Depressants/metabolism ; Ethanol/metabolism ; Humans ; Intestines/*microbiology ; Lipopolysaccharides/physiology ; Liver Diseases, Alcoholic/*microbiology ; Microbiota/*physiology ; Permeability

Bacterial Translocation ; physiology ; Humans ; Intestinal Mucosa ; pathology ; physiology ; Lipopolysaccharides ; metabolism ; physiology ; Liver Failure, Acute ; etiology ; immunology ; physiopathology ; Lymphocytes ; immunology ; metabolism ; Macrophages ; immunology ; metabolism ; Signal Transduction ; genetics ; physiology ; Toll-Like Receptor 4 ; metabolism ; physiology

OBJECTIVETo investigate the potential effect of bifidobacterial supplement on intestinal mucosal immunity associated with severe burns.

METHODSWistar rats were randomly divided into burn control group (BC group, n = 30), treatment group (BT group, n = 30), and sham-burn group (NC group, n = 10). Rats in BT group were fed bifidobacterial preparation (5 x 10(9) CFU/ml) after 30% total body surface area full-thickness burns, 1.5 ml, twice daily. Rats in BC group and NC group were fed normal saline, 1.5 ml, twice daily. Samples were taken on post-burn 1-, 3-, and 5-day. The incidence of bacterial translocation and bifidobacteria counts in the cecum mucosa were determined with standard methods. The sIgA levels in the mucus of the small intestine were measured by RIA. The positive sIgA expression in the lamina propria was detected by immunohistochemical staining.

RESULTSThe incidence of bacterial translocation was 42% and 16% in BC and BT groups on post-burn day 3 (P = 0.004), 30% and 8% on day 5 (P = 0.002), respectively. Plasma endotoxin levels were markedly higher in BC and BT groups than in NC group at the early stage post-burn. There was a significant decrease between BT group and BC group on post-burn day 1 (P = 0.0412). Bifidobacteria counts in cecum mucosa were reduced by 10- to 60-fold after thermal injury, but there was a remarkable increase in bifidobacteria counts in animals fed with bifidobacteria. sIgA levels in the intestinal mucus were significantly decreased in group BC, but they returned to normal range in BT group on post-burn day 5. Similarly, sIgA expression in the lamina propria was also weakened after burns, and had a tendency to recover after prescription of a 5-day bifidobacteria-supplemented formula. A strong positive correlation was observed between the counts of bifidobacteria in the cecal mucosa and the levels of sIgA in the intestinal mucus (r = 0.7534, P = 0.0000).

CONCLUSIONSThe expression and excretion of sIgA in the intestine appear to be markedly inhibited following a severe thermal injury. The supplement of exogenous bifidobacteria could improve sIgA formation in the small intestine, thereby reducing the incidence of bacterial/endotoxin translocation secondary to major burns.

Animals ; Bacterial Translocation ; Bifidobacterium ; physiology ; Burns ; immunology ; microbiology ; Disease Models, Animal ; Female ; Immunoglobulin A, Secretory ; biosynthesis ; Intestinal Mucosa ; immunology ; microbiology ; Male ; Probiotics ; Random Allocation ; Rats ; Rats, Wistar

OBJECTIVETo investigate the potential role of intestinal bifidobacteria in the pathogenesis of gut-origin bacteria/endotoxin translocation in scalded rats.

METHODSWistar rats inflicted with 30% III degree scalding on the back were employed as the model with the rats undergoing sham injury as the control. The intestinal bacteria/endotoxin translocation and the changes in cecal mucosal microflora were determined by routine methods. And the plasma IL-6 concentration was measured with ELISA.

RESULTSThe incident of bacterial translocation into internal organs increased markedly in scalded rats (P = 0.001). The plasma LPS levels on 1, 3 and 5 postburn days (PBDs) in scalded rat group were much higher than those in sham injury group. The number of bifidobacteria decreased sharply 20 - 250 fold, the fungi increased 5 - 60 fold and E. coli increased 0.5 - 30 fold in the caecal mucosal microflora in the scalding group. The ratio of bifidobacteria to E. coli in the scalding group (4 - 800:1) was much lower than that in the sham injury group (25000:1). Furthermore, the plasma IL-6 level increased evidently in the scalding group. It was indicated by further analysis that compared with the rats without bacterial translocation, the bifidobacteria decreased 120 fold, the fungal number increased 50 fold and the E. coli number increased 30 fold in the scalded rats. The bifidobacterial number in the caecal mucosal microflora was negatively correlated with the plasma concentrations of IL-6 and LPS (P < 0.01) in the scalding rat group, and the plasma concentration of IL-6 was significantly and positively correlated with that of LPS.

CONCLUSIONSevere scalding injury could lead to an the imbalance of intestinal microflora and the increased intestinal translocation of bacteria and LPS. The decrease of the ratio and number of bifidobacteria in the caecal mucosal microflora might be a contribute to the occurrence of postburn intestinal bacteria/endotoxin translocation.

Animals ; Bacterial Infections ; blood ; microbiology ; Bacterial Translocation ; physiology ; Bifidobacterium ; isolation & purification ; physiology ; Burns ; microbiology ; Colony Count, Microbial ; Escherichia coli ; isolation & purification ; physiology ; Female ; Interleukin-6 ; blood ; Intestines ; microbiology ; Kidney ; microbiology ; Lipopolysaccharides ; metabolism ; Liver ; microbiology ; Lymph Nodes ; microbiology ; Male ; Rats ; Rats, Wistar ; Spleen ; microbiology ; Time Factors

OBJECTIVETo study the protective effects of sacral nerve root electrostimulation on intestinal mechanical barrier in rats with spinal cord injury (SCI).

METHODSFifty six Wistar rats were divided into normal group, SCI control group and SCI group with sacral nerve root electrostimulation (8 rats in each subgroup at 24, 48, 72 h after spinal cord injury). The following experiments were performed respectively in rats from the 3 groups: bacteria culture from intestinal mesentery lymph nodes, liver, spleen, intestinal morphology observation and detection the protein expression level of ZO-1.

RESULTSThe intestinal mucosa appeared different degree of damage in SCI control group; cell-cell connections between intestinal epithelial cells were destroyed; Endotoxin levels in blood and the number of bacterial translocation increased obviously. Sacral nerve stimulation was found toimprove the intestinal mucosal, reduce the endotoxin content in the blood to normal level and the decrease the incidences of bacterial translocation of the gut origin. The expression of tight junction protein ZO-1 of rat intestinal tissue had no statistical differences among the 3 groups. On the other hand, the distribution of tight junction protein ZO-1 appeared different degrees of scattered and irregular in the control group while that in the experimental group appeared different degree of improvement as determined by the immunohistochemistry of rat intestinal tissue.

CONCLUSIONsacral nerve root electrostimulation can rehabilitate the peristalsis of denervated colon, promote defeacation and decrease bacterial amount, protection of the intestinal mechanical barrier between intestinal epithelial cells and tight junction, reducing the endotoxin content in the blood and suppressing bacterial translocation from the gut.

Animals ; Bacterial Translocation ; Electric Stimulation Therapy ; Endotoxins ; blood ; Epithelial Cells ; cytology ; Intestinal Mucosa ; physiology ; Peristalsis ; Rats ; Rats, Wistar ; Spinal Cord ; Spinal Cord Injuries ; physiopathology ; Zonula Occludens-1 Protein ; metabolism

BACKGROUNDDamage to the gut barrier often occurs during critical illnesses. In such cases, it is very important to alleviate impairment of the intestinal barrier and protect intestinal barrier function. This study investigated the protective effect of growth hormone on intestinal barrier function in rats under stress.

METHODSThis study consisted of prospective, randomized, and controlled animal experiments. Twenty-five Sprague-Dawley rats served as total parenteral nutrition (TPN) models and were divided into three groups: TPN group, sepsis (Sep) group, and growth hormone (GH) group. Another 8 rats served as normal controls. Each group received different stress stimuli. Rats were fed for 7 days, and samples were taken for examination 24 hours after gavaging with dual saccharides.

RESULTSThe architecture of the small intestinal mucosa in the Sep group showed the most severe damage among all groups. Nitric oxide levels in blood plasma and immunoglobulin A levels in the intestinal mucosa of the GH group were significantly lower than in the Sep group (P < 0.02). There were no significant changes in CD3 counts and in the CD4/CD8 ratio between the four groups. Dual sugar tests and bacteriological examinations revealed that intestinal permeability and rate of bacterial translocation in the GH group were lower than in the Sep group (P < 0.01, respectively).

CONCLUSIONProphylactic treatment with growth hormone can alleviate damage to intestinal barrier function caused by trauma and endotoxemia in rats under stress.

Animals ; Bacterial Translocation ; drug effects ; Growth Hormone ; therapeutic use ; Intestinal Mucosa ; drug effects ; physiology ; Parenteral Nutrition, Total ; adverse effects ; Prospective Studies ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Stress, Physiological ; physiopathology

OBJECTIVE: To observe the effect of chloroquine on the apoptosis of intestinal mucosa epithelial cell and enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion in rats. METHODS: The rat total hepatic ischemia-reperfusion model was built by blocking the hepatic portal, suprahepatic and infrahepatic vena cava for 20 minutes. Ninety Sprague-Dawley rats were assigned randomly into the sham operation group (Group A, n = 30), total hepatic ischemia-reperfusion treatment group (Group B, n = 30), and chloroquine administrated group (Group C, n = 30). Each group was subdivided randomly into 3 subgroups (n = 10) according to different experiment time phases as follows: after 20 minutes of total hepatic vascular exclusion (T0), 4 hours after reperfusion (T1), and the 48 hours of survival. Group A and Group B were intravenously injected with normal saline 1 mL/kg while Group C received chloroquine 10 mg/kg which dissolved in 1 mL/kg normal saline intravenously. The levels of portal blood D-lactate, TNF-alpha, endotoxin, and the intestinal mucosa MDA concentration were measured at T0 and T1; the portal blood, mesenteric lymph node, and spleen tissues were cultured for bacteria; and the apoptotic index of intestinal mucosa epithelial cells at T0 and T1 and the survival rate after 48 hour reperfusion were obtained. RESULTS: Compared with Group A, the levels of portal blood D-lactate, TNF-alpha, endotoxin and the intestinal mucosa MDA in Group B and Group C were significantly higher (P < 0.05 or P < 0.01). These indexes of Group C were lower than those of Group B (P < 0.05). The portal vein blood, mesenteric lymph node and spleen tissues existed the bacterium translocation both in Group B and Group C, and the positive rate in Group C was lower than that in Group B (P < 0.05). Apoptotic index of the intestinal mucosa epithelial cell increased significantly in Group B (P < 0.01) and Group C (P < 0.05), but the apoptotic index in Group C was lower than that in Group B (P < 0.05); the 48 hour survival rate of the rats in Group C was higher than that in group B (P < 0.05). CONCLUSION Chloroquine may decrease the intestinal mucosa epithelial cell apoptosis and the enterogenous bacteria-endotoxin translocation after total hepatic ischemia-reperfusion and increase the survival rate of the rats.
Animals ; Bacterial Translocation ; drug effects ; Chloroquine ; pharmacology ; Epithelial Cells ; pathology ; Escherichia coli ; physiology ; Female ; Intestinal Mucosa ; pathology ; Intestine, Small ; microbiology ; pathology ; Liver ; blood supply ; Male ; Phospholipases A ; antagonists & inhibitors ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; microbiology ; pathology

OBJECTIVETo investigate the plasma glutamine (Gln) level and relationships between the intestinal mucosal permeability and bacterial translocation and between bacterial translocation and systemic inflammatory response syndrome (SIRS) after abdominal operation.

METHODSThe peripheral blood was collected from 42 patients before and 2 and 7 days after elective abdominal operation. The plasma Gln concentration and lactulose/mannitol (L/M) ratio were measured and the whole blood bacterial DNA concentration was determined by polymerase chain reaction (PCR). The relationship between intestinal mucosal barrier dysfunction and the occurrence of postoperative SIRS was analyzed.

RESULTSThe plasma Gln level was significantly lowered (P<0.01) and L/M ratio increased (P<0.01) in these patients 2 and 7 days after the operation in comparison with the preoperative level. No bacterial DNA was detected before surgery, but PCR yielded positive results in 4 patients (9.5%, 4/42) at 2 days and in another patient at 7 days (2.4%, 1/42) after the operation. The 4 patients with positive PCR results 2 days after the operation showed significantly lower plasma Gln concentration (P<0.01) and higher L/M ratio (P<0.01) than those with negative results. SIRS occurred in 24 patients after surgery, whose plasma Gln level was significantly lower (P<0.01) and L/M ratio significantly higher (P<0.01) than that in the SIRS-free patients 2 days after the operation. Five of the 26 SIRS patients showed positive PCR results, while none of the 16 non-SIRS patients were positive, but this difference was not statistically significant (P>0.05).

CONCLUSIONDecreased plasma Gln and increased intestinal mucosal permeability are closely related to postoperative bacterial translocation and the intestinal mucosal barrier dysfunction, which may contribute to the occurrence of postoperative infection.

Abdomen ; surgery ; Adolescent ; Adult ; Aged ; Bacterial Translocation ; physiology ; DNA, Bacterial ; blood ; Female ; Glutamine ; blood ; Humans ; Intestinal Absorption ; Intestinal Mucosa ; metabolism ; physiopathology ; Intestine, Small ; metabolism ; physiopathology ; Male ; Middle Aged ; Permeability ; Postoperative Complications ; metabolism ; Stress, Physiological ; Systemic Inflammatory Response Syndrome ; etiology ; physiopathology ; Young Adult