Bacterial Translocation In Rats Research Articles

Lactobacillus reuteri improves function of the intestinal barrier in rats with acute liver failure through Nrf-2/HO-1 pathway

Objectives: We aimed to explore whether Lactobacillus reuteri could have a positive role in reducing inflammation and bacterial translocation in rats with acute liver failure. MethodsLactobacillus reuteri were gavaged to Sprague–Dawley (SD) rats at a dose of 1 × 109 CFU/mL once a day for 14 d. D-galactosamine was injected intraperitoneally to induce acute liver failure for 24 h on the 15th day. Liver function, liver and ileum histology, intestinal cytokines, intestinal tight junction proteins, lipopolysaccharide binding protein, apoptosis molecules, and nuclear factor erythroid-derived 2 (Nrf-2) / heme oxygenase (HO-1) molecules were assessed. ResultsThe results showed that L. reuteri alleviated liver injury and intestinal inflammation induced by D-galactosamine. L. reuteri also improved the expression of intestinal tight junction proteins and maintained the integrity of the intestinal barrier by inhibiting apoptosis of intestinal epithelial cells. L reuteri induced an increase in Nrf-2 nuclear translocation and elevated induction of HO-1. L. reuteri treatment significantly enhanced the expression of phosphoinositide 3-kinase/protein kinase B (PI3 K/Akt), protein kinase C (PKC), and their phosphorylated forms but not mitogen-activated protein kinase. The nuclear factor kappa B (NF-κB) pathway was inhibited after L. reuteri treatment. Interleukin (IL)-17A produced by Th17 cells and γδT17 cells may not contribute to an improved function of the intestinal barrier in L. reuteri–treated SD rats. ConclusionsOverall, our study indicated that L. reuteri–induced expression of intestinal tight junction proteins is mediated by the PI3 K/Akt-Nrf-2/HO-1-NF-κB and PKC-Nrf-2/HO-1-NF-κB pathways, which leads to inhibition of the apoptosis of intestinal epithelial cells, thus maintaining the integrity of the damaged intestinal barrier.

Altered intestinal microflora and barrier injury in severe acute pancreatitis can be changed by zinc.

To investigate the effect of zinc (Zn) supplementation on intestinal microflora changes and bacterial translocation in rats with severe acute pancreatitis (SAP), the rats were divided into the sham surgery (SS), SAP, SS + Zn, and SAP + Zn groups. Saline (0.1 mL/100g) and 5% sodium taurocholate were injected into the pancreaticobiliary duct of the rats in the SS and SAP + Zn groups, respectively. Intraperitoneal injection of 5 mg/kg Zn was performed immediately after injecting saline or 5% sodium taurocholate into the rats in both groups. Serum amylase and Zn levels, plasma endogenous endotoxin, intestinal permeability, and the positive rate of intestinal bacterial translocation were detected, haematoxylin and eosin (H&E) staining was performed, and the pancreatic tissue scores were calculated for each group. In addition, immunohistochemical (IHC) staining was performed to evaluate the expression of IL-1β and TNF-α. Real-time fluorescence quantitative PCR was used to quantify the gene copy numbers of Escherichia, Bifidobacterium, and Lactobacillus in the cecum. The levels of amylase and plasma endotoxin in the SAP group were significantly higher than those in the SS and SS + Zn groups. Intestinal mucosal permeability and intestinal bacterial translocation in the liver, pancreas, and mesenteric lymph nodes were increased in the SAP group. However, the levels of amylase and plasma endotoxin were decreased as a result of zinc supplementation in the SAP group. The expression of IL-1β and TNF-α was also reduced to a greater degree in the SAP + Zn group than in the SAP group. Moreover, alleviated intestinal mucosal permeability and intestinal bacterial translocation in the liver, pancreas, and mesenteric lymph nodes were found in the SAP + Zn group. The results of real-time quantitative PCR showed that the gene copy number of Escherichia increased with time, and the gene copy numbers of Lactobacillus and Bifidobacterium decreased over time. Zn supplementation prevented the release of TNF-α and IL-1β, alleviated intestinal permeability and endotoxemia, reduced bacterial translocation, and inhibited changes in pathogenic intestinal flora in rats with SAP.

Effect of Neotype Rectal Mild Hypothermia Therapy on Intestinal Bacterial Translocation in Rats with Hypoxic-Ischemic Brain Damage.

BackgroundPrevious studies have shown that a neotype rectal cooling device can induce mild hypothermia (MH) in Sprague-Dawley rats with ischemic-hypoxic brain damage (HIBD) and inhibit cell apoptosis in the hippocampal CAl region, and does not cause damage to rectal tissues. The present study aimed to investigate the effect of rectal MH on bacterial translocation (BT) in Sprague-Dawley rats with HIBD.Material/MethodsA total of 60 Sprague-Dawley rats were randomly divided into 4 groups: a control group (group C), a normothermia group (group NT), a cooling blanket group (group CB), and a rectal cooling group (group RC). Rats in group CB and group RC received MH using a cooling blanket and rectal cooling device after HIBD model establishment. Then, we measured diamine oxidase (DAO) and D-lactate level separately in groups NT, CB, and RC. Finally, the spleen, liver, and mesenteric lymph nodes were collected for bacterial culture, and rectal tissues were collected for H&E staining.ResultsThe therapeutic outcome was better in Sprague-Dawley rats receiving rectal MH without rectal injury compared to rats in group CB. Escherichia coli (E. coli) was found in MLNs in group RC. E. coli, Proteus vulgaris, Stenotrophomonas maltophilia, and Acinetobacter lwoffii were detected in the rats of groups CB and NT. At 12 h following rectal MH, DAO and D-lactate levels were lower than in group NT.ConclusionsThe neotype rectal MH cooling method could be a potential strategy to induce rapid, controllable hypothermia, thus reducing the possibility of inflammatory cell infiltration and BT incidence.

Intestinal Immune Dysregulation Driven by Dysbiosis Promotes Barrier Disruption and Bacterial Translocation in Rats With Cirrhosis.

In cirrhosis, intestinal dysbiosis, intestinal barrier impairment, and systemic immune system abnormalities lead to gut bacterial translocation (GBT) and bacterial infection. However, intestinal immune system dysfunction and its contribution to barrier damage are poorly understood. This study correlates immune system dysregulation in the intestines of rats at different stages of CCl4 -induced cirrhosis with barrier function and pathogenic microbiota. The following variables were addressed in the small intestine: intraepithelial lymphocyte (IEL) and lamina propria lymphocyte (LPL) activation status and cytokine production (flow cytometry), cytokine mRNA and protein expression (quantitative real-time PCR and immunofluorescence), microbiota composition of ileum content (16S recombinant DNA massive sequencing), permeability (fecal albumin loss), and epithelial junctions (immunohistochemistry and immunofluorescence). The intestinal mucosa in rats with cirrhosis showed a proinflammatory pattern of immune dysregulation in IELs and LPLs, which featured the expansion of activated lymphocytes, switch to a T helper 1 (Th1) regulatory pattern, and Th17 reduction. In rats with cirrhosis with ascites, this state was associated with epithelial junction protein disruption, fecal albumin loss, and GBT. Direct correlations (P < 0.01) were observed between elevated interferon gamma (IFNγ)-expressing T cytotoxic LPLs and fecal albumin and between inflammatory taxa abundance and IFNγ-producing immune cells in the ileum. Bowel decontamination led to redistributed microbiota composition, reduced proinflammatory activation of mucosal immune cells, normalized fecal albumin levels, and diminished GBT; but there were no modifications in Th17 depletion. Conclusion: The intestinal mucosa of rats with cirrhosis acquires a proinflammatory profile of immune dysregulation that parallels the severity of cirrhosis; this impaired intestinal immune response is driven by gut dysbiosis and leads to disrupted barrier function, promoting GBT.

Abstract P-315: EFFECT OF NEOTYPE RECTAL MILD HYPOTHERMIA COOLING METHOD ON INTESTINAL BACTERIAL TRANSLOCATION IN HYPOXIC-ISCHEMIC BRAIN DAMAGE

Aims & Objectives: Neotype rectal mild hypothermia cooling method was designed previously. The present study investigated the effect on bacterial translocation in rats with hypoxic-ischemic brain damage. Methods Design: A total of 60 male rats were randomly divided into group control, normothermia, cooling blanket, and rectal cooling. Plasma diamine oxidase (DAO) and D-lactate were measured separately at 0, 12, and 24h after HIBD. Spleen, liver, mesenteric lymph nodes (MLN) and rectum tissue were harvested and analyzed. Setting and Participants: Children’s hospital of Chongqing Medical University located in China. Interventions: Group CB was interfered by cooling blanket, and group RC interfered by rectal cooling. Results The integrity of the rectum tissue of rats in group RC was superior to that of CB and NT groups with less inflammatory infiltration under mucosa in the former group. Escherichia coli was found in the culture plate containing tissues of MLN in the RC group. On the other hand, Escherichia coli, Proteus vulgaris, Stenotrophomonas maltophilia, and Acinetobacter lwoffii were detected in culture plates containing tissues of MLN, spleen, and liver in NT and CB groups. The concentration of DAO and D-lactate decreased at 12h in group RC, which was predominant than that in group CB, and increased at 24h in both RC and CB groups (P<0.05). Conclusions Neotype rectal mild hypothermia cooling method could be a potential therapeutic strategy to maintain the integrity of rectal histology and intestinal microecology,reduce the possibility of inflammatory cell attack, intestinal mucosal permeability, and BT incidence.

Fermented milk containing Lactobacillus paracasei subsp. paracasei CNCM I-1518 reduces bacterial translocation in rats treated with carbon tetrachloride

Probiotics can prevent pathological bacterial translocation by modulating intestinal microbiota and improving the gut barrier. The aim was to evaluate the effect of a fermented milk containing Lactobacillus paracasei subsp. paracasei CNCM I-1518 on bacterial translocation in rats with carbon tetrachloride (CCl4)-induced cirrhosis. Sprague-Dawley rats treated with CCl4 were randomized into a probiotic group that received fermented milk containing Lactobacillus paracasei subsp. paracasei CNCM I-1518 in drinking water or a water group that received water only. Laparotomy was performed one week after ascites development. We evaluated bacterial translocation, intestinal microbiota, the intestinal barrier and cytokines in mesenteric lymph nodes and serum. Bacterial translocation decreased and gut dysbiosis improved in the probiotic group compared to the water group. The ileal β-defensin-1 concentration was higher and ileal malondialdehyde levels were lower in the probiotic group than in water group. There were no differences between groups in serum cytokines but TNF-α levels in mesenteric lymph nodes were lower in the probiotic group than in the water group. Fermented milk containing Lactobacillus paracasei subsp. paracasei CNCM I-1518 decreases bacterial translocation, gut dysbiosis and ileal oxidative damage and increases ileal β-defensin-1 expression in rats treated with CCl4, suggesting an improvement in the intestinal barrier integrity.

Use of molecular typing to investigate bacterial translocation from the intestinal tract of chlorpyrifos-exposed rats.

BackgroundHuman are confronted on a daily basis with contaminant pesticide residues in food, water and other components of the environment. Although the digestive system is the first organ to come into contact with food contaminants, very few data are available on the impact of low-dose pesticide exposure during the in utero and postnatal periods on intestinal bacterial translocation (BT). Previous studies have revealed that chlorpyrifos (CPF) exposure is associated with intestinal dysbiosis and the contamination of sterile organs. Here, molecular typing was used to investigate intestinal bacterial translocation in rats exposed to chlorpyrifos in utero and during lactation. The translocated bacteria were profiled, and CPF tolerance and antibiotic resistance traits were determined.MethodsA total of 72 intestinal segments and extra-intestinal organs were obtained from 14 CPF-exposed rats. The samples were cultured to isolate bacterial strains that had tolerated treatment with 1 or 5 mg CPF/kg bodyweight/day in vivo. Strains were identified using matrix-assisted laser desorption/ionization (MALDI) Biotyper. The disk diffusion method was used to determine the antibiotic susceptibility. The isolates were genotyped with PCR assays for the enterobacterial repetitive intergenic consensus sequence and random amplification polymorphic DNA.ResultsBacterial translocation was confirmed for 7 of the 31 strains (22.6 %) isolated from extra-intestinal sites. Overall, the most prevalent bacteria were Staphylococcus aureus (55.5 % of the 72 intestinal and extra-intestinal isolates), Enterococcus faecalis (27.7 %) and Bacillus cereus (9.8 %). 5 % of the S. aureus isolates displayed methicillin resistance. Seventy two strains were identified phenotypically, and seven translocated strains (mainly S. aureus) were identified by genotyping. Genotypically confirmed translocation was mainly observed found in pesticide-exposed groups (6 out of 7).ConclusionBT from the intestinal tract colonized normally sterile extra-intestinal organs in CPF-exposed rats. Our findings validate the use of molecular typing for the assessment of intestinal BT in CPF-exposed rats during critical periods of development.

Su1202 Immunomodulation by Hypoxic Preconditioning Prevents Mesenteric Ischemia/Reperfusion-Induced Bacterial Translocation in Rats: Role of TNFα-Dependent Neutrophil Priming

Su1202 Immunomodulation by Hypoxic Preconditioning Prevents Mesenteric Ischemia/Reperfusion-Induced Bacterial Translocation in Rats: Role of TNFα-Dependent Neutrophil Priming

The Kampo medicine “Daikenchuto (TU-100)” prevents bacterial translocation and hepatic fibrosis in a rat model of biliary atresia

Biliary atresia is the most common cause of end-stage liver disease in children. It is known that bile duct ligation contributes to liver fibrosis via bacterial translocation (BT) and toll-like receptor 4 (TLR4) signaling of hepatic stellate cells (HSCs). We have reported previously that the traditional Japanese medicine, "Dai-kenchu-to (TU-100)," a form of "Kampo medicine" prevents BT in rats exposed to the stress of fasting. The aim of this study was to clarify the effect of TU-100 on a rat model of biliary atresia using bile duct ligation. Bile duct ligation and subsequent daily oral administration of TU-100 was performed in 6-week-old rats. The rats were killed at 3, 7, or 14days after bile duct ligation to evaluate the liver injury, occurrence of BT, and hepatic fibrosis. As an invitro experiment, we isolated fresh HSCs from the rats undergoing bile duct ligation. After cell attachment, TU-100 and its 3 component herbs (eg, processed ginger, ginseng radix, and Japanese pepper) were added, and the expressions of Alpha actin2 (acta2), Alpha-1 type I collagen (colIa1), and tissue inhibitor of metalloproteinase 1 (timp1) were analyzed. Invivo experiments demonstrated that oral administration of TU-100 decreased liver injury and atrophy of intestinal mucosa BT, hepatic fibrosis, and hepatic expression of alpha smooth muscle actin (αSMA) and TLR4, compared with rats that underwent bile duct ligation only. Invitro experiments showed that administration of TU-100 or the component herbs inhibited the expressions of acta2, colIa1, and timp1 in the HSCs. TU-100 prevented BT, activation of HSCs, and subsequent hepatic fibrosis. TU-100 may prevent progression of hepatic fibrosis in children with biliary atresia and improve prognosis.

FRI-009 - Intestinal Bacterial Translocation in Rats with Cirrhosis is Related to Intestinal Immune Dysfunction

FRI-009 - Intestinal Bacterial Translocation in Rats with Cirrhosis is Related to Intestinal Immune Dysfunction

P0088 : Fermented milk containing Lactobacillus paracasei subsp. paracasei CNCM I -1518 reduces bacterial translocation in rats treated with CCL4

P0088 : Fermented milk containing Lactobacillus paracasei subsp. paracasei CNCM I -1518 reduces bacterial translocation in rats treated with CCL4

Long-term cannabinoid type 2 receptor agonist therapy decreases bacterial translocation in rats with cirrhosis and ascites

Intestinal hyperpermeability, impaired peritoneal macrophages (PMs) phagocytosis, and bacterial translocation (BT), resulting in increased systemic and local infection/inflammation such as spontaneous bacterial peritonitis (SBP) together with increased tumor necrosis factor-α (TNFα) levels, are all implicated in the pathogenesis of cirrhosis-related complications. Manipulation of the cannabinoid receptors (CB1R and CB2R), which are expressed on the gut mucosa and PMs, has been reported to modulate intestinal inflammation and systemic inflammatory cytokine release. Our study aims to explore the effects of chronic CB1R/CB2R agonist/antagonist treatments on relevant abnormalities in cirrhotic ascitic rats. Vehicle, archidonyl-2-chloroethylamide (ACEA, CB1R agonist), JWH133 (CB2R agonist), and AM630 (CB2R antagonist) were given to thioacetamide (TAA) and common bile duct ligation (BDL) cirrhotic rats with ascites for two weeks and various measurement were performed. Compared to sham rats, CB2Rs were downregulated in cirrhotic rat intestines and PMs. The two-week JWH133 treatment significantly decreased systemic/intestinal oxidative stress, TNFα and inflammatory mediators, infection, intestinal mucosal damage and hyperpermeability; the JWH133 treatment also decreased bacterial overgrowth/adhesion, BT and SBP, upregulated intestinal tight junctions and downregulated the PM TNFα receptor/NFκBp65 protein expression in cirrhotic rats. Acute and chronic JWH133 treatment corrected the TNFα-induced suppression of phagocytosis of cirrhotic rat PMs, which then could be reversed by concomitant AM630 treatment. Our study suggests that CB2R agonists have the potential to treat BT and various relevant abnormalities through inhibition of systemic/intestinal oxidative stress, inflammatory cytokines and TNFα release in cirrhosis. Overall, the chronic CB2R agonist treatment affects multiple approach mechanisms, and its direct effect on the hyperdynamic circulation is only minor.

VSL#3 probiotic treatment decreases bacterial translocation in rats with carbon tetrachloride-induced cirrhosis.

Probiotics can prevent pathological bacterial translocation in cirrhosis by modulating intestinal microbiota and improving gut barrier and immune disturbances. To evaluate the effect of probiotic VSL#3 on bacterial translocation, intestinal microbiota, gut barrier and inflammatory response in rats with experimental cirrhosis. Forty-six Sprague-Dawley rats with CCl4 -induced cirrhosis were randomized into two groups: VSL#3 group (n = 22) that received VSL#3 in drinking water, and water group (n = 24) that received water only. Treatment began at week 6 of cirrhosis induction and continued until laparotomy, performed 1 week after development of ascites or at week 20. A control group included 11 healthy rats. At this study end, we evaluated bacterial translocation, intestinal flora, intestinal barrier (ileal claudin-2 and 4, β-defensin-1, occludin and malondialdehyde as index of oxidative damage) and serum cytokines. Mortality during this study was similar in the VSL#3 group (10/22, 45%) and the water group (10/24, 42%) (P = 1). The incidence of bacterial translocation was 1/12 (8%) in the VSL#3 group, 7/14 (50%) in the water group (P = 0.03 vs. VSL#3 group) and 0/11 in the control group (P = 0.008 vs. water group). The concentration of ileal and caecal enterobacteria and enterococci was similar in the two groups of cirrhotic rats. The ileal occludin concentration was higher and ileal malondialdehyde and serum levels of TNF-α were lower in the VSL#3 group than in the water group (P < 0.05). VSL#3 decreases bacterial translocation, the pro-inflammatory state and ileal oxidative damage and increases ileal occludin expression in rats with experimental cirrhosis.

Hypertonic Saline Solution Reduces Mesenteric Microcirculatory Dysfunctions and Bacterial Translocation in a Rat Model of Strangulated Small Bowel Obstruction

We examined the effects of hypertonic saline (HS) on inflammatory, metabolic variables, and bacterial translocation (BT) in rats submitted to intestinal obstruction and ischemia (IO). Male Wistar rats were submitted to IO and treated, 2 h thereafter, with lactated Ringer's (LR) (4 mL/kg per 5 min, i.v.) or HS (7.5% NaCl, 4 mL/kg per 5 min, i.v.). Twenty-four hours after IO, rats were also submitted to enterectomy/enteroanastomosis to resection of necrotized small bowel. Leukocyte-endothelial interactions were investigated by intravital microscopy and the expression of P-selectin and intercellular adhesion molecule 1 by immunohistochemistry. Bacterial cultures of mesenteric lymph nodes, liver, spleen, and blood were used to evaluate BT. Levels of chemokines (cytokine-induced neutrophil chemoattractants 1 and 2), insulin, and corticosterone were determined by enzyme-linked immunosorbent assay. Intestinal histology, serum urea and creatinine levels, and hepatic enzymes activities were performed to evaluate local and remote damage. Relative to IO and LR-treated rats, which exhibited increases in the number of rolling (1.5-fold), adhered (3.5-fold) and migrated (9.0-fold) leukocytes, and increased expression of P-selectin (3-fold) and intercellular adhesion molecule 1 (3-fold) on mesenteric microcirculation, treatment with HS followed by enterectomy reduced leukocyte-endothelial interactions and expression of both adhesion molecules to values attained in sham rats. Serum chemokines were normalized after treatment with both solutions followed by enterectomy. Hypertonic saline-treated rats demonstrated a significant reduction in BT to 50% in liver and spleen samples and bacteremia (14%), compared with 82% of BT in liver and spleen samples of IO and LR-treated rats and bacteremia (57%). Local intestinal damage was attenuated, and renal and hepatic function preserved by treatment with HS followed by enterectomy. Survival rate increased to 86% up to 15 days. Data presented suggest that HS solution followed by enterectomy reduces mesenteric microcirculatory dysfunctions and BT, attenuating local and remote damage in a model of strangulated small bowel obstruction.

Use of in vivo caspase inhibitor in rat burn and infection injury prevents gut bacterial translocation and modulates CD4+ T cell effector immune response. (P3272)

Abstract Our previous studies have focused on gut-associated lymphoid tissues, failure of intestinal gut barrier, bacterial translocation, and sepsis exploring the roles of antigen-presenting cells, DCs, CD4+ T cell and regulatory T cells in immunosuppression following acute burn and/or burn-plus-infection injury. In an established rodent model of burn plus infection we tested in vivo use of caspase inhibitor and studied T cell effector immune response and gut barrier function. Z-VAD-FMK, a highly specific, cell-permeable, and irreversible inhibitor of caspases was given to rats and were then assessed for mortality, bacterial translocation, T cell receptor expression and apoptosis. The results suggested an increase in CD4+CD25+ T cell phenotype in splenocytes of burn as compared to sham rats, however such an elevation in CD4+CD25+ expression was reduced in CLP and CLP+Burn+Caspase-Inhibitor groups. The results also showed that there was an increase in adhesion receptors (LFA) and decrease in CD62L in burn, whereas no difference in these adhesion receptor expressions was ascertained in Burn+CLP and Burn+CLP+Caspase-Inhibitor treated rats. A decrease in homing receptor (CD49d) was also noticed in Burn+CLP and Burn+CLP+Caspase-Inhibitor-treated animals. The Colony Forming Unit (CFU) results showed absence of bacterial translocation in rats that were subjected to burn+CLP+Caspase-Inhibitor, however there was significant bacterial translocation in rats from the group of CLP and burn only.

Regional Sympathetic Blockade Attenuates Activation of Intestinal Macrophages and Reduces Gut Barrier Failure

Endotoxin-induced activation of monocytes may lead to extravasation of cells, excessive production of nitric oxide, and subsequent epithelial injury in the gut. Regional sympathetic blockade by means of thoracic epidural anesthesia has been implicated to protect the epithelial barrier. This study tested the hypothesis that thoracic epidural anesthesia decreases epithelial permeability by attenuating monocytic production of nitric oxide and nitrosative stress. Rats were anesthetized, hemodynamically monitored, and mechanically ventilated. Endotoxemia was induced by an intravenous bolus injection of Escherichia coli lipopolysaccharide. Either lidocaine 2% or normal saline was injected as a bolus, followed by a continuous infusion via an epidural catheter. Three hundred minutes after injection of lipopolysaccharide or normal saline, gut epithelial permeability to fluorescein isothiocyanate-dextran (4 kDa), intestinal expression of inducible nitric oxide synthase by macrophages, and lipid peroxidation represented by 8-isoprostane tissue concentration were quantified. Thoracic epidural anesthesia significantly attenuated the endotoxin-induced increases in gut epithelial permeability (437 [293, 492] vs. 628 [532, 1,042] ng/ml, median [quartiles], P = 0.03), expression of nitric oxide synthase (2 [1,2] vs. 7 [5,8] cells per 384 µm(2), P = 0.003), macrophage infiltration, and lipid peroxidation (22,460 ± 11,476 vs. 37,840 ± 17,551 pg/ml, mean ± SD, P = 0.05). Thoracic epidural anesthesia attenuates endotoxin-induced gut epithelial injury. This is likely due to a decrease in monocytic extravasation and intestinal nitrosative stress. As possible mechanisms, direct nerve-immune interplay, a reduction in plasma catecholamines, or a systemic lidocaine effect has to be considered.

Beneficial effect of splenic artery ligation on bacterial translocation after major liver resection in rats

ObjectiveIn major liver resection, bacterial translocation appears to be an important mechanism in the pathogenesis of spontaneous infection. This study was designed to investigate the effects of splenic artery ligation on bacterial translocation after major liver resection. Materials and methodsRats were divided into three groups: the sham operation group (SO group), the two-thirds partial hepatectomy group (PHx group) and the two-thirds partial hepatectomy plus splenic artery ligation group (PHx+Sp group). Bacterial translocation, endotoxemia, d-lactic acid and intestinal histology were analyzed among three groups. ResultsThe rate of bacterial translocation was higher in the PHx rats than in the SO rats (65.0% vs. 6.67%; P=0.001), so that in the PHx+Sp rats (25.0%; P=0.011). Endotoxemia was not evident in the SO rats (0pg/ml) and blood endotoxin levels decreased in the PHx+Sp rats (1.47pg/ml) compared with the PHx rats (4.05pg/ml, P<0.001). d-lactic acid was also higher in both the PHx and PHx+Sp rats compared with the SO rats (39.09mg/ml, 23.36mg/ml, and 1.68mg/ml; P<0.01). ConclusionSplenic artery ligation enhanced intestinal barrier function and diminished blood endotoxin levels and bacterial translocation in rats with major liver resection.

Role of TLR4/NF-κB in Damage to Intestinal Mucosa Barrier Function and Bacterial Translocation in Rats Exposed to Hypoxia

The role of Toll-like receptor 4 (TLR4)/nuclear factor-kappa-B (NF-κB) in intestinal mucosal barrier damage and bacterial translocation under hypoxic exposure is unclear. Here, we investigated their role using an acute hypobaric hypoxia model. Adult Sprague-Dawley rats were divided into control (C), hypoxia (H), hypoxia+NF-κB inhibitor pyrrolidinedithiocarbamic acid (PDTC) (100 mg. kg) (HP), hypoxia+0.5 mg/kg lipopolysaccharide (HPL), and hypoxia+PDTC+LPS (HPL) group. Except control group, other four groups were placed in a hypobaric chamber set at 7000 m. Samples were collected at 72 h after pressure reduction. Damage in ultrastructure of the intestinal tract was examined by transmission electron microscopy and bacterial translocation was detected by cultivation. Kinetic turbidimetric assay was used to measure the serum LPS.ELISA was performed to detect TNF-α and IL-6 serum concentrations. Fluorescent quantitative RT-PCR was used to measure TLR4 mRNA levels was measured using quantitative RT-PCR and protein of NF-κB p65 was measured by western blotting. Different degrees of intestinal mucosa damage were observed in groups H and HL. The damage was significantly alleviated after blockage of the TLR4/NF-κB signaling pathway. PDTC- treatment also reversed hyoxia- and LPS-induced bacterial translocation rate and increased serum levels of LPS, TNF-α, and IL-6. TLR4 mRNA levels and NF-κB p65 expression were consistent with the serum factor results. This study suggested that TLR4 and NF-κB expression increased in rat intestinal tissues after acute hypoxia exposure. PDTC-treatment reversed TLR4 and NF-κB upregulation and alleviated damage to the intestinal tract and bacterial translocation. Thus, the TLR4/NF-κB signaling pathway may be critical to the mechanism underlying hypoxia-induced damage to intestinal barrier function and bacterial translocation.

Implantation de la microflore intestinale et régulation de la translocation bactérienne sous l’effet d’un traitement au citrate de caféine chez le raton en période néonatale

To relieve respiratory problems such as apnea in newborns, caffeine citrate is the drug of choice because of its good tolerance and therapeutic index. However, its impact on the intestinal microbial ecosystem and on bacterial translocation in the neonatal period remains insufficiently investigated. Therefore, the objective of this study was to evaluate the effects of caffeine citrate on the establishment of the intestinal microflora and bacterial translocation in rats from birth to the 30th day of life. Newborn Wistar rats were divided into four groups of 14 animals, each subdivided into a control group receiving a placebo (12mL tap water/kg/day) and another treated with caffeine citrate (12mg/kg/day). The animals were nursed by their mothers and weighed daily. A group of 14 rats was killed at birth and after 10, 20, or 30 days of life. Organs in which translocation was assessed (liver, lungs, spleen, and kidneys) and various fragments of intestine (duodenum, jejunum, ileum, and colon) were surgically removed. The bacteriological analysis performed involved enumeration of the total microflora, staphylococci, enterobacteria, and lactobacilli. From the 10th day, caffeine was shown to significantly decrease the weight of treated animals as compared with controls (P<0.05). However, caffeine treatment did not drastically alter the kinetics of establishment of the intestinal microflora as only enterobacteria were found to be significantly lower in any intestinal segment of the treated group (P<0.05). Moreover, from the 20th day of life, caffeine citrate significantly downregulated bacterial translocation of both Gram-positive and -negative bacteria (P<0.05). This preliminary study on the effects of treatment with caffeine citrate may open opportunities in clinical pediatrics; the treatment will remain partially effective in preventing bacterial translocation in the neonatal period.

Role of quorum sensing Escherichia coli regulator C in intestinal bacterial translocation in rats subjected to hemorrhagic shock

Objective To investigate the role of quorum sensing Escherichia coli regulator C (qseC) in intestinal bacterial translocation in rats subjected to hemorrhagic shock.Methods Thirty Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 5 groups (n =6 each):control group (group C),MC1000-sham shock group (group M-SS),MC1000qseC-sham shock group (group △-SS),MC1000-hemorrhagic shock group (group M-HS),and MC1000△ qseC-hemorrhagic shock group (group △-HS).The rats drank 150 μg/ml of disinfect water containing streptomycin in 3 consecutive days to inhibit the autochthonous flora in the intestinal tract.From 4th day,the rats were fed with Escherichia Coli MC1000 or MC1000△ qseC 1 ml/100 g by gastric perfusion once a day for another 3 consecutive days in the other 4 groups,while the rats were fed with normal saline instead in group C.Hemorrhagic shock was induced by blood-letting.The mesenteric lymph node (MLN),spleen and liver specimens were obtained at 24 h after operation for bacterial culture and the bacteria were identified.Bacterial translocation from gut to MLN,spleen and liver was observed and the number of bacteria in MLN,spleen and liver tissues were counted.Results The rate of bacterial translocation was significantly higher,and the number of bacterial colonies in MLN,spleen and liver tissues and the total number of bacterial colonies were significantly larger in groups M-HS and △-HS than in group C,and in group M-HS than in groups M-SS and △-SS (P ＜ 0.05).The rate of bacterial translocation was significantly lower,and the number of bacterial colonies in MLN,spleen and liver tissues and the total number of bacterial colonies were significantly smaller in group △-HS than in group MHS.Conclusion QseC is involved in the intestinal bacterial translocation following hemorrhagic shock in rats. Key words: Escherichia coli; Shock,hemorrhagic; Bacterial translocation; Intestines