Nitric oxide-derived urinary nitrate as a marker of intestinal bacterial translocation in rats

Oudenhoven, I. M. J.; Klaasen, H. L. B. M.; Lapré, J.A.; Weerkamp, Ah; Meer, Roelof van der

doi:10.1016/0016-5085(94)90059-0

Cited by 51 publications

(30 citation statements)

References 24 publications

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“…The virulence of each strain was sustained by routine oral passage in Reg3b ϩ/Ϫ mice and subsequent isolation of the pathogen from extraintestinal organs. S. enteritidis was grown on brilliant green agar modified (BGAM) plus sulfamandalate supplement (Oxoid, Basingstoke, United Kingdom) and quantified as described previously (18). L. monocytogenes was grown and enumerated by similar culturing methods using Palcam agar (28) plus Palcam selective supplement (Oxoid).…”

Section: Methodsmentioning

confidence: 99%

Intestinally Secreted C-Type Lectin Reg3b Attenuates Salmonellosis but Not Listeriosis in Mice

et al. 2012

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Section: Methodsmentioning

confidence: 99%

Intestinally Secreted C-Type Lectin Reg3b Attenuates Salmonellosis but Not Listeriosis in Mice

et al. 2012

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“…The spleen, mesenteric lymph nodes, and the liver were excised, homogenised in sterile saline, and plated on Modified Brilliant Green Agar (Oxoid) to quantify viable salmonella, as described previously. 15 In addition, the ileum (last 12 cm proximal to the ileocaecal valve), caecum, and colon were pulled out, longitudinally excised, and freed of their contents by extensive washing in sterile saline. The mucosa of these intestinal segments was scraped off using a spatula.…”

Section: Analysis Of Nitric Oxide Metabolites In Urinementioning

confidence: 99%

Dietary fructo-oligosaccharides and lactulose inhibit intestinal colonisation but stimulate translocation of salmonella in rats

Bovee‐Oudenhoven

Bruggencate²,

Lettink-Wissink³

et al. 2003

Gut

130

100

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Background and aims: It is frequently assumed that dietary non-digestible carbohydrates improve host resistance to intestinal infections by stimulating the protective gut microflora. However, compelling scientific evidence from in vivo infection studies is lacking. Therefore, we studied the effect of several nondigestible carbohydrates on the resistance of rats to Salmonella enteritidis infection. Methods: Rats (n = 8 per group) were fed ''humanised'' purified diets containing 4% lactulose, fructooligosaccharides (FOS), resistant starch, wheat fibre, or cellulose. After an adaptation period of 2 weeks the animals were orally infected with S enteritidis. Supplement induced changes in faecal biochemical and microbiological parameters were studied before infection. Colonisation of salmonella was determined by studying the faecal excretion of this pathogen and translocation by analysis of urinary nitric oxide metabolites over time and classical organ cultures. Intestinal mucosal myeloperoxidase activity was determined to quantify intestinal inflammation after infection. Results: Despite stimulation of intestinal lactobacilli and bifidobacteria and inhibition of salmonella colonisation, FOS and lactulose significantly enhanced translocation of this pathogen. These supplements also increased cytotoxicity of faecal water and faecal mucin excretion, which may reflect mucosal irritation. In addition, caecal and colonic, but not ileal, mucosal myeloperoxidase activity was increased in infected rats fed FOS and lactulose. In contrast, cellulose, wheat fibre, and resistant starch did not affect the resistance to salmonella. Conclusions: In contrast to most expectations, FOS and lactulose impair the resistance of rats to intestinal salmonella infection. Obviously, stimulation of the endogenous lactobacilli and bifidobacteria is no guarantee of improved host defence against intestinal infections.

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“…While NO is an unstable molecule, one means of investigating NO for mation is to measure nitrite (NO 2 -), which is one of two primar y stable nonvolatile breakdown products of NO. A dose dependent increase in nitrite has been demonstrated to occur when macrophages are activated with lipopolysaccharide (LPS) both in vitro and in vivo [20] . Therefore, we speculated that endotoxin mediated increases in the NO metabolite nitrite in urine are related to the magnitude of intestinal macromolecular permeability and hence to LC related complications.…”

Section: N I T R I C O X I D E ( N O ) H a S A R O L E I N C I R R H mentioning

confidence: 99%

Increased intestinal macromolecular permeability and urine nitrite excretion associated with liver cirrhosis with ascites

Lee¹,

Son²,

Han³

et al. 2008

WJG

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AIM:To determine intestinal permeability, the serum tumor necrosis factor (TNF)-α level and urine nitric oxide (NO) metabolites are altered in liver cirrhosis (LC) with or without ascites. METHODS: Fifty-three patients with LC and 26 healthy control subjects were enrolled in the study. The intestinal permeability value is expressed as the percentage of polyethylene glycol (PEG) 400 and 3350 retrieval in 8-h urine samples as determined by high performance liquid chromatography. Serum TNF-α concentrations and urine NO metabolites were determined using an enzyme-linked immunosorbent assay (ELISA) and Greiss reaction method, respectively. RESULTS: The intestinal permeability index was significantly higher in patients with LC with ascites than in healthy control subjects or patients with LC without ascites (0.88 ± 0.12 vs 0.52 ± 0.05 or 0.53 ± 0.03, P < 0.05) and correlated with urine nitrite excretion (r = 0.98). Interestingly, the serum TNF-α concentration was significantly higher in LC without ascites than in control subjects or in LC with ascites (198.9 ± 55.8 pg/mL vs 40.9 ± 12.3 pg/mL or 32.1 ± 13.3 pg/mL, P < 0.05). Urine nitrite excretion was significantly higher in LC with ascites than in the control subjects or in LC without ascites (1170.9 ± 28.7 μmol/L vs 903.1 ± 55.1 μmol/L or 956.7 ± 47.7 μmol/L, P < 0.05). CONCLUSION:Increased intestinal macromolecular permeability and NO is probably of importance in the pathophysiology and progression of LC with ascites, but the serum TNF-α concentration was not related to LC with ascites.

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Nitric oxide-derived urinary nitrate as a marker of intestinal bacterial translocation in rats

Cited by 51 publications

References 24 publications

Intestinally Secreted C-Type Lectin Reg3b Attenuates Salmonellosis but Not Listeriosis in Mice

Intestinally Secreted C-Type Lectin Reg3b Attenuates Salmonellosis but Not Listeriosis in Mice

Dietary fructo-oligosaccharides and lactulose inhibit intestinal colonisation but stimulate translocation of salmonella in rats

Increased intestinal macromolecular permeability and urine nitrite excretion associated with liver cirrhosis with ascites

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