2.Bacterial Translocation in Liver Cirrhosis.
The Korean Journal of Hepatology 2005;11(3):218-226
No abstract available.
*Bacterial Translocation
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Humans
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Liver Cirrhosis/*microbiology
3.The gut-origin infection in severe burns.
Chinese Journal of Burns 2008;24(5):331-333
Early in 1962, after an extensive review including 312 cases of bacteremia in burn patients, we were surprised to find that there was about 30% of bacteremia in the patients who had no detectable microorganisms from repeated wound cultures, but blood cultures were usually positive for gut flora. From that time on the idea of gut-origin infection emerged. In following twenty years, a series of experiments were carried on in Wistar rats with 30% TBSA full-thickness burn. The results showed that the fluorescein labeled enteric microbes (Pseudomonas aeruginosa, Bacteroid fragilis and Candida albicans) could translocate through the stress injured intestinal wall and were recovered in visceral organs. The radioisotope 125I labeled endotoxin began to ascend in concentration in portal vein since 15 minutes postburn. Radioautography of liver sections demonstrated the labeled endotoxin granules. With the creation of minute mesenteric lymph fistulas, the clearance of endotoxin and TNFalpha was found to be significantly high in lymph fluid exited from the intestine. All above evidences indicated that the gut is a potential route of endogenous infection, and it also explained how did the patients manifest sepsis early after burn injury without a definite infectious focus. Now the concepts of gut-origin infection are commonly accepted, the measures like early enteral feeding for the protection of intestinal barrier has been established.
Bacteremia
;
etiology
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Bacterial Translocation
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Burns
;
microbiology
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Gastrointestinal Tract
;
microbiology
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Humans
4.The change of intestinal microecology in rats after orthotopic liver transplantation.
Mei-hong YU ; Xiu-li YU ; Chun-lei CHEN ; Liang-hui GAO ; Wei-lin MAO ; Dong YAN ; Yu CHEN ; Ji-fang SHENG ; Lan-juan LI ; Shu-sen ZHENG
Chinese Journal of Surgery 2008;46(15):1139-1142
OBJECTIVETo investigate the intestinal microflora status and bacterial translocation in rats after liver transplantation.
METHODSMale Brown-Norway (BN) rats were randomly divided into 4 groups: group I (n = 8) for liver transplantation; group II (n = 8) for simulated liver transplantation; group III (n = 8) for sham operation and group IV (n = 8) for normal group. Caecal bacterial counts, plasma endotoxin, intestinal mucosal ultrastructure and bacterial translocation to liver, spleen, kidney, and mesenteric lymph node were studied 24 h after surgery.
RESULTSThe numbers of Bifidobacterium and Lactobacillus per gram of wet feces were significantly decreased in group I compare with those in the group III and group IV, while Enterobacteriaceae and Enterococcus counts were increased markedly compare with those in the group III and group IV, but no different was found between group I and group II. Impaired intestinal mucosa integrity were found in the group I and group II. In group I, the levels of plasma endotoxin increased after the transplantation when compare with group III and group IV. Increased incidence of bacterial translocation to liver, spleen and mesenteric lymph node were also observed after the transplantation (compare with those in the group IV, P < 0.01; compare with those in the group III, P < 0.01, P < 0.01, P < 0.05, separately). The increased rate of the bacterial translocation in liver was also found in transplantation group as compare with group II (P < 0.05).
CONCLUSIONSLiver transplantation may lead to disturbance of intestinal microflora and impairment of intestinal mucosal barrier function, and this dysfunction might be caused by the process of intestinal ischemia-reperfusion injury in transplantation.
Animals ; Bacterial Translocation ; Endotoxins ; blood ; Intestines ; microbiology ; ultrastructure ; Liver Transplantation ; Male ; Random Allocation ; Rats
5.The Effect of Surgical Manipulation on the Bacterial Translocation from the Gut.
Chong Suk KIM ; Hoon Bae JEON ; Jin Woo RYU ; Kwang Ho KIM ; Bum Whan KOO
Journal of the Korean Surgical Society 1997;52(6):790-795
The bacterial translocation is defined as the passage of viable bacteria or its toxin from the lumen of the gastrointestinal tract through the intestinal mucosa to other site of host. It is believed that bacterial translocation may lead to systemic infection and septicemia. The purpose of this study was to determine what factors in experimental surgical trauma lead to bacterial translocation. Two-nonth-old Wistar albino rats were divided into three groups: A-control; B-anesthesia only and C-anesthesia and surgery. After 24 and 48 hours, caval blood, mesenteric lymph nodes, liver, lung and spleen were harvested aseptically and cultured for aerobic organism. To exclude the possibility of contamination during surgical manipulation and harvesting, swab culture of peritoneal surface was performed. The bacterial translocation seldom occurred 24 hours after surgical manipulation. There was a significant increase in the number of animals with bacterial translocation in group C, 48 hours after manipulation and harvesting, swab culture of peritoneal surface was performed. The bacterial translocation seldom occurred 24 hours after surgical manipulation. There was a significant increase in the number of animals with bacterial translocation in group C, 48 hours after surgical manipulation. The majority of translocating bacteria was E. coli.
Animals
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Bacteria
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Bacterial Translocation*
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Gastrointestinal Tract
;
Intestinal Mucosa
;
Liver
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Lung
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Lymph Nodes
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Rats
;
Sepsis
;
Spleen
6.Destructive Intestinal Translocation of Vibrio vulnificus Determines Successful Oral Infection.
Seol Hee HONG ; Kwangjoon JEONG ; Mi Jin PARK ; Youn Suhk LEE ; Tra My Duong NU ; Soo Young KIM ; Joon Haeng RHEE ; Shee Eun LEE
Journal of Bacteriology and Virology 2013;43(4):262-269
Vibrio vulnificus causes primary septicemia as a result of the consumption of contaminated seafood. The intestinal epithelial layer is the first host barrier encountered by V. vulnificus upon oral intake; however, epithelial translocation (invasion) of V. vulnificus has not been extensively studied. In this study, we investigated in vivo translocation of V. vulnificus using clinical (CMCP6) and environmental isolates (96-11-17M). And we analyzed physiological changes of intestinal epithelium concurrent with bacterial translocation by using polarized HCA-7 transwell culture system. The efficiency of epithelial translocation of 97-11-17M strains was significantly lower than that of pathogenic clinical isolate CMCP6 in a murine ligated ileal loop model. In an oral infection model, the survival rate was reciprocally related with efficacy of in vivo epithelial translocation. These results indicate that efficient translocation of V. vulnificus through intestinal epithelium is highly correlated with successful oral infection. We determined translocation of the bacteria from upper to lower chamber, changes of transepithelial electric resistance (TER) and cytotoxicity of the polarized HCA-7 cells to understand general features of V. vulnificus invasion. Bacterial translocation was accompanied by big decrease of TER (about 90%) and about 50% cytotoxicity of the epithelial cells. Taken together, these results indicate that V. vulnificus actively translocates the epithelium by destruction of epithelium and the efficiency of intestinal invasion by V. vulnificus is critical for successful oral infection. From this result, it is suggested that integrity of intestinal barrier is an important factor for susceptibility to oral infection of V. vulnificus.
Bacteria
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Bacterial Translocation
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Electric Impedance
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Epithelial Cells
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Epithelium
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Intestinal Mucosa
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Seafood
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Sepsis
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Survival Rate
;
Vibrio vulnificus*
;
Vibrio*
7.Pathogenesis of Acute Pancreatitis.
Korean Journal of Medicine 2013;85(2):111-115
Acute pancreatitis is an inflammatory disease that is caused by various etiologies including gallstone, alcohol or hypertriglyceridemia. Although most cases of acute pancreatitis show self-limiting course, severe cases are still associated with significant morbidity and mortality. The pathogenic mechanisms of acute pancreatitis are not fully understood. However, it is a central dogma that premature intracellular activation of trypsinogen is the earliest pathologic event. Even though it remains unknown how intracellular trypsinogen activation can be caused by such diverse etiologies, this initial insult in pancreatic acinar cells lead to local inflammatory complications and a systemic response or death. Pathophysiologic mechanisms related to the progression of acute pancreatitis include microcirculatory injury, chemoattraction of inflammatory cells, release of pro-inflammatory cytokines, and bacterial translocation to pancreas and systemic circulation. Recently, several interesting transgenic mice model experiments shed a light in trypsin independent mechanism of local and systemic inflammation for progression of acute pancreatitis.
Acinar Cells
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Animals
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Bacterial Translocation
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Cytokines
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Gallstones
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Hypertriglyceridemia
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Inflammation
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Light
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Mice
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Mice, Transgenic
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Pancreas
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Pancreatitis
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Trypsin
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Trypsinogen
8.The Effects of Increased Intra-Abdominal Pressure on Bacterial Translocation.
Coskun POLAT ; Orhan Cem AKTEPE ; Gokhan AKBULUT ; Sezgin YILMAZ ; Yuksel ARIKAN ; Osman Nuri DILEK ; Ozcan GOKCE
Yonsei Medical Journal 2003;44(2):259-264
In this study, we investigated the effect of different values of intra-abdominal pressure on bacterial translocation. Twenty-four Wistar-Albino rats were divided into four groups. The animals belonging to the Control group were not subjected to any increased intra-abdominal pressure. In groups I, II and III, an intra-abdominal pressure of 14, 20, and 25 mmHg, respectively, was established by carbon dioxide pneumoperitoneum for a period of 60 minutes. Four hours after the pneumoperitoneum, all animals were sacrificed to evaluate the degree of bacterial translocation at this time. Liver, spleen and mesenteric lymph nodes were excised under sterile conditions. Bacterial growth was assessed using standard bacteriological techniques and compared statistically. The Kruskal-Wallis and Mann-Whitney U tests were used for the statistical analysis. Different amounts of bacterial growth were found in all of the animals subjected to increased intra-abdominal pressure, except for the controls. Bacterial translocation was detected at an intra-abdominal pressure of 14 mmHg but this finding was not statistically significant (p > 0.05). There was a significant increase in bacterial growth in animals subjected to an intra- abdominal pressure of 20 mmHg or above (p < 0.001). As a result, we found that bacterial translocation started when the intra-abdominal pressure reached a level of 14 mmHg. Patients should be closely monitored for septic complication risks following laparoscopic procedures in which the intra-abdominal pressure exceeds 20 mmHg.
Abdomen
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Animals
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*Bacterial Translocation
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Carbon Dioxide
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Laparoscopy/*adverse effects
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Pneumoperitoneum, Artificial/adverse effects
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Pressure
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Rats
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Rats, Wistar
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Splanchnic Circulation
9.Role of lymphatics in bacterial translocation from intestine in burn rats.
Yong-Qiang FENG ; De-Chang WANG ; Kun WANG ; Xiang-Feng LENG ; Hu XIAO ; Dan-Feng GUO
Chinese Journal of Burns 2011;27(1):49-53
OBJECTIVETo investigate the role of lymphatics in bacterial translocation from intestine of rats with burn.
METHODSEscherichia coli (E. coli) labeled with chloromethylbenzamidodialkylcarbocyanine (CM-DIL) were prepared. Sixty adult male Wistar rats were randomly divided into scald group and sham injury group according to the envelope method, with 30 rats in each group. Rats in both groups were gavaged with 0.5 mL fluid containing CM-DIL-labeled E. coli. Rats in scald group were inflicted with 30% TBSA deep partial-thickness scald (verified by pathological section) and resuscitated with fluid. Rats in sham injury group were sham injured by bathing in 25 degrees C water for 10 s (verified by pathological section) and also received with fluid infusion. Mesenteric lymph node (MLN), liver, mesenteric lymph fluid (MLF), and liver vein blood (LVB) were harvested at post injury hour (PIH) 2, 24, and 72. Bacteria translocation was detected with fluorescent tracing technique and bacteria culture. The endotoxin content in above-mentioned four kinds of specimens was quantitatively determined with chromogenic substrate limulus amebocyte lysate. The carrying capacity of endotoxin in MLF and LVB was calculated. Data were processed with t test or one-way analysis of variance.
RESULTS(1) Living bacteria were in short-stick form, and they were seen moving in single or in doubles or triples in sample fluid. Dead bacteria were in irregular aggregates. Labeled bacteria in small amount were detected in sham injury group, their number peaked at PIH 24. A large amount of labeled bacteria were detected in scald group at PIH 2, which peaked at PIH 24 and decreased at PIH 72. The largest amount of labeled bacteria were found in MLN in scald group as compared to those in the other samples, and the number peaked at PIH 24 [(5872 +/- 1976) x 10(3) CFU/g], which was obviously higher than that [(216 +/- 110) x 10(3) CFU/g, t = 30.129, P = 0.000] in sham injury group. The number of bacteria decreased at PIH 72, but it was still significantly different from that in sham injury group ( t = 4.323, P = 0.000). The number of bacteria in LVB was the smallest. (2) 29 (24.2%) samples out of the 120 samples in sham injury group were positive for bacteria. 72 (60.0%) samples out of the 120 samples in scald group were positive for bacteria. No alive bacterium was detected at any time point in LVB sample in both group; the other three samples were detected with alive bacteria since PIH 2. There were more alive bacteria detected in MLN and liver as compared with the other two kinds of samples in scald group. The amount of bacteria in MLN, liver, and MLF in scald group were higher than those in sham injury group (with t value respectively 4.353, 4.354, 4.965, P values all equal to 0.000). (3) The endotoxin level in each kind of sample at each time point was obviously higher in scald group than that in sham injury group, and it peaked at PIH 2 in liver and MLF. The difference of endotoxin level among 4 kinds of samples in scald group at PIH 2 was statistically significant ( F = 258.47, P = 0.000), and the endotoxin level was higher in liver, MLN, and MLF. They were obviously higher than those in sham injury group (with t value respectively 43.378, 43.123, 22.423, P values all equal to 0.000). The endotoxin level in MLF was 9 times of that in LVB. (4) The carrying capacity of endotoxin in LVB and MLF at each time point in scald group was higher than that in sham injury group.
CONCLUSIONSCM-DIL marked bacteria can reflect the microbial translocation condition. The lymphatic route is an important pathway for bacteria translocation.
Animals ; Bacterial Translocation ; Burns ; microbiology ; Intestinal Mucosa ; microbiology ; Lymph Nodes ; microbiology ; Lymphatic System ; microbiology ; Lymphatic Vessels ; Male ; Rats ; Rats, Wistar