Literature DB >> 17339238

Probiotic treatment of rat pups normalises corticosterone release and ameliorates colonic dysfunction induced by maternal separation.

Mélanie G Gareau1, Jennifer Jury, Glenda MacQueen, Philip M Sherman, Mary H Perdue.   

Abstract

BACKGROUND: We previously showed that neonatal maternal separation (MS) of rat pups causes immediate and long-term changes in intestinal physiology. AIM: To examine if administration of probiotics affects MS-induced gut dysfunction.
METHODS: MS pups were separated from the dam for 3 h/day from days 4 to 19; non-separated (NS) pups served as controls. Twice per day during the separation period, 10(8) probiotic organisms (two strains of Lactobacillus species) were administered to MS and NS pups; vehicle-treated pups received saline. Studies were conducted on day 20, when blood was collected for corticosterone measurement as an indication of hypothalamus-pituitary-adrenal (HPA) axis activity, and colonic function was studied in tissues mounted in Ussing chambers. Ion transport was indicated by baseline and stimulated short-circuit current (Isc); macromolecular permeability was measured by flux of horseradish peroxidase (HRP) across colonic tissues; and bacterial adherence/penetration into the mucosa was quantified by culturing tissues in selective media. Colonic function and host defence were also evaluated at day 60.
RESULTS: Isc and HRP flux were significantly higher in the colon of MS versus NS pups. There was increased adhesion/penetration of total bacteria in MS pups, but a significant reduction in Lactobacillus species. Probiotic administration ameliorated the MS-induced gut functional abnormalities and bacterial adhesion/penetration at both day 20 and 60, and reduced the elevated corticosterone levels at day 20.
CONCLUSIONS: The results indicate that altered enteric flora are responsible for colonic pathophysiology. Probiotics improve gut dysfunction induced by MS, at least in part by normalisation of HPA axis activity.

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Year:  2007        PMID: 17339238      PMCID: PMC2095679          DOI: 10.1136/gut.2006.117176

Source DB:  PubMed          Journal:  Gut        ISSN: 0017-5749            Impact factor:   23.059


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