Literature DB >> 8612416

Characteristics of the intestinal epithelial barrier during dietary manipulation and glucocorticoid stress.

J C Spitz1, S Ghandi, M Taveras, E Aoys, J C Alverdy.   

Abstract

OBJECTIVES: a) To determine the significance of stress-induced alterations in intestinal permeability by measuring the transmucosal flux of formyl-methionyl-leucyl-phenylalanine (f-MLP), a ubiquitous neutrophilic chemoattractant present in the human and rodent colon; and b) to determine whether stress and/or diet influence(s) bacterial adherence-induced changes in epithelial permeability by affecting the production of secretory immunoglobulin A (IgA), the main immune mechanism preventing bacterial adherence.
DESIGN: Prospective, randomized, controlled study.
SETTING: University animal research laboratory.
SUBJECTS: Female Fischer rats.
INTERVENTIONS: Rats were randomly assigned to four groups of seven animals each. Groups of animals were assigned to receive saline or dexamethasone (0.8 mg/kg ip) and were either starved (5% dextrose in water ad libitum) or fed (water and rat chow) for 48 hrs.
MEASUREMENTS AND MAIN RESULTS: Mucosal barrier function was evaluated by measuring secretory IgA, bacterial adherence to the intestinal mucosa, and transepithelial electrical resistance, a measure of tight junction permeability. The f-MLP permeation across the mucosa was also determined in segments with significant permeability changes. Results indicate that starvation in dexamethasone-treated rats significantly impairs secretory IgA, promotes bacterial adherence to the mucosa, and results in increased intestinal permeability to f-MLP. These effects are significantly attenuated by the feeding of rat chow.
CONCLUSIONS: Alterations in intestinal barrier function are characterized by depressed IgA, bacterial adherence to the intestinal mucosa, and permeation of clinically relevant proinflammatory luminal macromolecules (f-MLP). Enteral stimulation with foodstuffs is a necessary protective measure to prevent altered epithelial barrier function during glucocorticoid stress.

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Year:  1996        PMID: 8612416     DOI: 10.1097/00003246-199604000-00015

Source DB:  PubMed          Journal:  Crit Care Med        ISSN: 0090-3493            Impact factor:   7.598


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