Bacterial Translocation in Short-Bowel Syndrome in Rats

Schimpl, G.; Feierl, Gebhard; Linni, K.; Uitz, Christiane; Özbey, Hüseyin; Höllwarth, Michael E.

doi:10.1055/s-2008-1072249

Cited by 37 publications

(17 citation statements)

References 7 publications

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“…The ''Principles of laboratory animal care'' (NIH publication No. 86-23, revised 1985) were followed and all experiments were conducted with the permission of the animal research commission of the Austrian Ministry of Science following local guidelines for the use and care of laboratory animals [5,18]. The rats were housed in an environmentally controlled vivarium with a 12 h lightdark cycle and received a standard pellet diet and water ad libitum.…”

Section: Methodsmentioning

confidence: 99%

The role of nuclear factor-kappa B in bacterial translocation in cholestatic rats

et al. 2005

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Xanthinoxidase (XO) derived radical species are involved in bacterial translocation (BT) in cholestatic rats. The mechanism by which XO influences remains unclear. It has been shown recently that nuclear factor-kappa B (NF-kappaB), a ubiquitous transcription factor, can be activated by oxidative stress and thereby promote the process of BT. We investigated the effects of NF-kappaB inactivation on the incidence of BT in cholestatic rats. Sprague-Dawley rats were randomly assigned to one of eight groups: groups 1-4 were sham laparotomized rats either untreated (S1) or treated for 5 days with thalidomide (S2), curcumin (S3), or Inchin-ko (ICK; S4); groups 5-8 underwent common bile duct ligation (CBDL) for 5 days and were either untreated (C1) or treated with thalidomide (C2), curcumin (C3), or ICK (C4). After 5 days bacteriological cultures were performed from portal blood and V. cava, from the central mesenteric lymph node complex (MLN), spleen, and liver. The intensity of the activated NF-kappaB-subunit p65/p50 in the ileum mucosa was estimated by light microscopy and a scoring system from 1 to 20. Malondialdehyde (MDA) and myeloperoxidase activity (MPO) in the ileum were evaluated and expressed as U/g dry weight. Thalidomide and ICK reduced in CBDL-rats significantly the BT rate (63% vs. 18%, 63% vs. 30%, P<0.01). Enzyme estimations (MDA, MPO, and GSH) in sham operated animals showed no significant changes in the untreated groups compared with the treated groups. CBDL-rats pre-treatment with all three compounds caused a significant increase of MDA levels if groups were compared with the untreated C1-group (C1 31.6+/-7.7, C2 54.5+/-12.2, C3 53.3+/-11.2, and C4 47.2+/-9.4). GSH was reduced after the pre-treatment by all compounds but only significantly after curcumin pre-treatment (C1 vs. C3: 13.9+/-1.8 vs. 7.1+/-1.8; P<0.05). MPO estimations were significantly higher in the untreated C1-group if compared with groups C2, C3, and C4 (C1 1036.4+/-340.9, C2 709.9+/-125.9, C3 545.2+/-136.6, and C4 556.7+/-247.4; P<0.05). Thalidomide inhibited significantly the activation of NF-kappaB (C2 vs. C1: 6.0+/-4.5 vs. 12.7+/-5.3; P<0.01). Likewise, Curcumin and ICK suppressed NF-kappaB activation, but this did not reach significance in this experiment. NF-kappaB is involved in the process of BT in cholestatic rats and may be activated by XO derived ROS. We assume that the activated NF-kappaB initiates transcription of target genes inducing cytokine production, which in turn disrupts the tight junctions leading to BT from the intestinal lumen to the MLNs and circulation.

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Section: Methodsmentioning

confidence: 99%

The role of nuclear factor-kappa B in bacterial translocation in cholestatic rats

et al. 2005

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“…Experimental studies using animal models have demonstrated that this kind of surgery leads to an increase in permeability of the remaining bowel (29) and bacterial translocation (30). These phenomena could be related to the absorption of endotoxins and bacterial lipopolysaccharides, increasing TNF-α levels and finally leading to steatohepatitis (31).…”

Section: Discussionmentioning

confidence: 99%

Lack of evidence for the pathogenic role of iron and HFE gene mutations in Brazilian patients with nonalcoholic steatohepatitis

Deguti

Sipahi

Gayotto

et al. 2003

Braz J Med Biol Res

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The hypothesis of the role of iron overload associated with HFE gene mutations in the pathogenesis of nonalcoholic steatohepatitis (NASH) has been raised in recent years. In the present study, biochemical and histopathological evidence of iron overload and HFE mutations was investigated in NASH patients. Thirty-two NASH patients, 19 females (59%), average 49.2 years, 72% Caucasians, 12% Mulattoes and 12% Asians, were submitted to serum aminotransferase and iron profile determinations. Liver biopsies were analyzed for necroinflammatory activity, architectural damage and iron deposition. In 31 of the patients, C282Y and H63D mutations were tested by PCR-RFLP. Alanine aminotransferase levels were increased in 30 patients, 2.42 ± 1.12 times the upper normal limit on average. Serum iron concentration, transferrin saturation and ferritin averages were 99.4 ± 31.3 g/dl, 33.1 ± 12.7% and 219.8 ± 163.8 µg/dl, respectively, corresponding to normal values in 93.5, 68.7 and 78.1% of the patients. Hepatic siderosis was observed in three patients and was not associated with architectural damage (P = 0.53) or with necroinflammatory activity (P = 0.27). The allelic frequencies (N = 31) found were 1.6 and 14.1% for C282Y and H63D, respectively, which were compatible with those described for the local population. In conclusion, no evidence of an association of hepatic iron overload and HFE mutations with NASH was found. Brazilian NASH patients comprise a heterogeneous group with many associated conditions such as hyperinsulinism, environmental hepatotoxin exposure and drugs, but not hepatic iron overload, and their disease susceptibility could be related to genetic and environmental features other than HFE mutations.

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“…The incidence of liver injury, cholestasis, and septic episodes may be reduced when measures are taken to reduce or modify bacterial levels in the gut lumen (25,36,59). In animal models of intestinal resection, an increased incidence of bacteria cultured from mesenteric lymph nodes has been demonstrated (40,44).…”

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Enterocyte apoptosis after enterectomy in mice is activated independent of the extrinsic death receptor pathway

Knott

O’Brien

Juno

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

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. Enterocyte apoptosis after enterectomy SBR in mice is activated independent of the extrinsic death receptor pathway. Am J Physiol Gastrointest Liver Physiol 285: G404-G413, 2003. First published April 30, 2003 10.1152/ajpgi.00096.2003.-Intestinal adaptation following small bowel resection (SBR) is associated with greater rates of enterocyte apoptosis by unknown mechanism(s). Because postresection adaptation is associated with increased translocation of luminal bacteria, we sought to characterize the role for the extrinsic, death receptor pathway for the activation of enterocyte apoptosis after massive SBR. We first performed SBR or sham operations in mice, and the temporal expression of caspases 8, 9, and 3, death receptors tumor necrosis factor receptor-1 (TNFR 1) and Fas and corresponding ligands (TNF and Fas ligand) was determined in the remnant intestine at various postoperative time points. Ileal TNFR 1 and Fas expression were then measured after SBR in the setting of increased (waved-2 mice) or decreased (exogenous EGF administration) apoptosis. Finally, intestinal adaptation and apoptosis were recorded in the remnant ileum after SBR in TNFR 1-null and Fas-null mice. The expression of death receptor family proteins and caspases demonstrated only modest changes after SBR and did not correlate with the histological appearance of apoptosis. In the setting of accelerated apoptosis, TNFR 1 and Fas expression were paradoxically decreased. Apoptotic and adaptive responses were preserved in both TNFR 1-null and Fas-null mice. These results suggest that the mechanism for increased enterocyte apoptosis following massive SBR does not appear to involve the extrinsic, death receptor-mediated pathway.

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Bacterial Translocation in Short-Bowel Syndrome in Rats

Cited by 37 publications

References 7 publications

The role of nuclear factor-kappa B in bacterial translocation in cholestatic rats

The role of nuclear factor-kappa B in bacterial translocation in cholestatic rats

Lack of evidence for the pathogenic role of iron and HFE gene mutations in Brazilian patients with nonalcoholic steatohepatitis

Enterocyte apoptosis after enterectomy in mice is activated independent of the extrinsic death receptor pathway

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