Publications by authors named "E A Vicuna"

Dextran sodium sulfate ( DSS: ) has been shown to be effective at inducing enteric inflammation in broiler chickens, resulting in increased leakage of orally administered fluorescein isothiocyanate dextran to circulation. In a previous study, 2 doses of DSS (0.45 g/dose) administered as oral gavage resulted in increased mucosal permeability.

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Enteric inflammation models can help researchers' study methods to improve health and performance and evaluate various growth promoters and dietary formulations targeted to improve performance in poultry. Oral administration of fluorescein isothiocyanate-dextran (FITC-d; 3-5 kDa) and its pericellular mucosal epithelial leakage are an established marker to evaluate enteric inflammation in multiple species. The present study evaluated different methods to induce gut inflammation in poultry based on FITC-d leakage.

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We have previously shown that intestinal barrier function can be adversely affected by poorly digested diets or feed restriction, resulting in increased intestinal inflammation-associated permeability. Three experiments were conducted in broilers to evaluate the effect of dexamethasone (DEX) treatment on systemic fluorescein isothiocyanate-dextran (FITC-D; 3-5 kDa) levels, indicative of increased gut epithelial leakage. Experiment 1 compared DEX injections of 1 mg/kg, once per day on d 3, 5, and 9, with feed administration at 0.

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Traditionally, antibiotic growth promoters (AGP) have been used in foodstock animals to reduce enteric inflammation and maintain intestinal homeostasis, thus improving growth and performance. Due to increasing restrictions regarding the use of AGP however, precise and high throughput enteric inflammation models and markers to search for effective alternatives are urgently needed. In this paper, oral administration of fluorescein isothiocyanate dextran (FITC-d, 3-5 kDa) and its passage into blood was used as a marker for tight junction permeability.

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Gut inflammation is a cardinal event occurring in various gastrointestinal diseases regardless of etiology. A potential mechanism of action for antibiotic growth promoters and probiotics is alleviation or attenuation of such inflammation. In vivo inflammation models and markers to quantify changes in inflammation, such as paracellular leakage and tight junction function, are necessary tools in the search for methods to reduce enteric inflammation.

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